The Truth About Health Care! – video 9:07 min.

Source: Uploaded by UndergroundWellness on Jan 28, 2011 to YouTube

Sean Crofton expresses his views about health care in America.

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Symtoms of Kidney Disease – Video 1:58 min.

Source: Uploaded by monkeyseevideos on May 28, 2010 to YouTube

To View the Next Video in this Series Please Click Here: http://www.monkeysee.com/play/16525-who-s-at-risk-for-kidney-disease

Caffeine’s Buzz Chases Away Women’s Depression, Study Finds

 

By Melissa Healy

Compared with uncaffeinated women, those who drank the equivalent of four or more cups of coffee a day are more likely to drink alcohol and smoke cigarettes and less likely to volunteer their time in church or community groups. But a new study finds that well-caffeinated women have a key health advantage over their more abstemious sisters: They’re less likely to become depressed.

In the back-and-forth world of research on caffeine’s effects, the latest study suggests that women who get several jolts of java a day may do more than get a quick boost: Their mental health may see sustained improvement even as the physical stresses of aging accumulate. Among a large population of women tracked for as long as 18 years each, the women who routinely consumed the highest levels of caffeine were 20 percent less likely than those who drank little to none to become depressed when they were nearing or in their 60s.

Coffee, which ounce-for-ounce delivers the strongest dose of caffeine, was most women’s pick-me-up of choice. And generally, the more caffeine a woman drank, the more likely she was to be in good mental health. The study was published Monday in the Archives of Internal Medicine.

“A small amount of coffee may keep you more active and more happy, and that may result in the long run in better brain health,” said Dr. Alberto Ascherio, the senior author of the study. Cautioning that his group’s findings are preliminary, Ascherio added that they should ease concerns among female coffee addicts as they enter midlife; the average age of the participants was 63 years in 1996, when researchers began tracking the incidence of depression among the women.

“There’s no reason, from what we know, for people to cut back on their coffee consumption, unless, of course, it makes them feel bad,” said Ascherio, professor of epidemiology and nutrition at Harvard University’s School of Public Health. Ascherio was the lead author of a 2003 study that linked high coffee consumption with lower rates of Parkinson’s disease in men, but not in women. That early study, however, did turn up one key warning for women: Among heavy coffee drinkers who had taken hormone replacement therapy, the likelihood of developing Parkinson’s disease rose.

To gauge the link between caffeine consumption and depression, the authors of the latest research drew upon the long-running Nurse’s Health Study. Some 53,739 women who participated in that larger study completed periodic surveys of their eating habits for 14 years. While women with a prior history of depression were included in the study, none of those participating showed significant depressive symptoms, or had a depression diagnosis in 1996, when the researchers began to measure depression rates.

In an effort to gauge caffeine’s long-term, rather than its immediate effect, researchers waited two years after a woman’s last dietary report to begin inquiries about her mental health. At that time also, they asked about health and lifestyle behavior, such as alcohol consumption, tobacco use, exercise, marital status and involvement in social or community groups. Then, at least twice over the next four-year period, they would ask her whether she had been diagnosed with depression or had begun taking antidepressant medication on a regular basis in either of the previous two years.

This article was published at NationofChange at: http://www.nationofchange.org/caffeines-buzz-chases-away-womens-depression-study-finds-1317229283. All rights are reserved.

Nutrition and Your Mental Health

Uploaded by psychetruth on Aug 13, 2007 to YouTube

Nutrition by Natalie
Nutrition and Your Mental Health

What does nutrition have to do with mental health? You might be surprised to find out the truth behind what happens when a person has a nutritional deficiency.

 
Nutritional deficiencies can cause all sorts of psychiatric symptoms including apathy, low energy, irritability, insomnia, low energy, agitation, fatigue, concentration problems, aches and pains, weight changes, including weight loss or weight gain. Sound a lot like the symptoms of depression? The truth is the average American diet of fast food is low in vital nutrition that you need for your body to function correctly.

This isn’t to say that all depression is caused by bad nutrition but it’s certainly a contributing factor in many cases and poor nutrition will always make depression worse. Antidepressant drugs also do not correct nutritional problems. So if your depressed because of nutritional problems an antidepressant will only partially cover up the problem and you body still won’t function correctly.

Nutrition vs. Conventional Medicine

Uploaded by psychetruth on Sep 21, 2007 to YouTube

Nutrition by Natalie

Nutrition vs. Conventional Medicine
Take A Pill

Americans are constantly being bombarded by pharmaceutical commercials with the message of take a pill.

High cholesterol, acid reflux, depression, insomnia, allergies, irritable bowel syndrome, shaking leg syndrome, social anxiety disorder, ADHD, GERDs, sexual dysfunction,; it doesn’t matter what’s wrong w/ you, big Pharma has a pill that’s right for you.

In this video Natalie discusses the different between the conventional medicine approach of just taking a pill to a preventative approach of health; nutrition.

 
This video discusses the three most profitable classes of drugs; Statins (Drug prescribed for high cholesterol), Proton Pump Inhibitors (drugs prescribed for heart burn, upset stomach or acid reflux disorder) and Antidepressants, prescribed for depression.

 
Common Statin drugs include Lovastatin, Simvastatin, Atorvastatin, Fluvastatin, Pravastatin and Rosuvastatin.

Common Proton Pump Inhibitors include, Aciphex, Prevacid, Nexium, Prilosec, Protonix, Zegerid and omeprazole.

Common Antidepressants include Prozac, Zoloft, Lexapro, Paxil, Luvox, Effexor, Cymbalta and Wellbutrin.

This video talks about common side effects of these three classes of drugs.
There may be more to your health than simply taking a pill.

Adult Acne – 3 Common Causes of Adult Acne Problems

 

By M. C. Johnson

1. Hormonal

Polycystic ovarian syndrome is a hormonal condition that causes irregular or absent menstrual periods because of irregularities of ovulation. Acne is also a common symptom of PMS (premenstrual syndrome), which is one of the most common manifestations of hormonal imbalance, affecting over half of all women. The hormonal fluctuations in women over 35 become more dramatic and unpredictable as they enter pre-menopausal and approach menopause, which can aggravate hormonal acne.

Many women who haven’t had a breakout since their teens or early twenties suddenly find themselves battling acne when they turn 40. Having acne when you’re in your forties can affect your self esteem. When you’re in you forties you’re already self conscious about those things that seem to be changing such as your skin and your energy level. You may even notice dark circles forming under your eyes. Therefore acne is not something that you want added to the list of problems.

2. Diet

Your diet matters when it comes to acne. Systemic inflammation is created by diets high in sugar, refined carbohydrates and trans fats, and low in antioxidants, which manifests itself in your skin in the form of acne. You should try to eat five portions of fruit and vegetables each day as part of a balanced diet, which should give you a mixture of nutrients and vitamins necessary to fight off free radicals. When I increased my intake of fruits and vegetables I found that I didn’t crave junk foods. My stomach would no longer handle fried greasy foods because I have changed my eating to include more fruits and vegetables and no fried foods.

Just recently I had not been able to go grocery shopping, therefore my fruit and vegetable intake was limited and my body new it wasn’t getting the fruits and vegetables that I was accustomed to giving it. Ones body will crave what it’s accustomed to being fed. If you constantly eat junk food then your body will get use to it. My body is now use to having fruits and vegetables and no fried foods and that’s what it craves. My skin is also clearer since I’ve changed my diet. Eating healthy foods will help get rid of acne.

3. Stress

Cortisol is an important hormone in the body; secreted by the adrenal glands and involved in inflammatory response. Your body produces cortisol when you’re stressed and unfortunately most women are burdened with constant, insisting stress, calling on the adrenal glands to constantly produce cortisol. Stress often plays a big part in the acne problem. When you are becoming tense, your adrenal glands work harder, filling your bloodstream with the hormone cortisol. This triggers the sweat glands on your face to produce more oil.

We should learn to alleviate stress by doing things that brings us comfort and joy. Do you enjoy reading inspirational books? After a stressful day why don’t you take time out to eliminate the stress. Perhaps, you like to play golf or bowl or even watch inspirational movies. If you’re the type of person that feels guilty for taking time for yourself, then think of it as a way to get rid of your acne. Stress also leads to other health problems. Therefore take time out to alleviate stress.

There are many different solutions for acne treatment. I prefer natural cures to any problem so that it would deal with the cause and get rid of the problem. You should want to get rid of acne and not just treat acne.

Martha Johnson has been a certified Herbal Specialist since December 2001 and has demonstrated the knowledge necessary to teach others about herbal nutrition and how to lead a healthier life.

http://theacnenaturaltreatment.blogspot.com

Article Source: http://EzineArticles.com/?expert=M._C._Johnson

Nerve Disease and Bladder Control

For the urinary system to do its job, muscles and nerves must work together to hold urine in the bladder and then release it at the right time. Nerves carry messages from the bladder to the brain to let it know when the bladder is full. They also carry messages from the brain to the bladder, telling muscles either to tighten or release. A nerve problem might affect your bladder control if the nerves that are supposed to carry messages between the brain and the bladder do not work properly.

What bladder control problems does nerve damage cause?

Nerves that work poorly can lead to three different kinds of bladder control problems.

Nerves carry signals from the brain to the bladder and sphincter.

Overactive bladder. Damaged nerves may send signals to the bladder at the wrong time, causing its muscles to squeeze without warning. The symptoms of overactive bladder include

• urinary frequency-defined as urination eight or more times a day or two or more times at night
• urinary urgency-the sudden, strong need to urinate immediately
• urge incontinence-leakage of urine that follows a sudden, strong urge to urinate

Poor control of sphincter muscles. Sphincter muscles surround the urethra and keep it closed to hold urine in the bladder. If the nerves to the sphincter muscles are damaged, the muscles may become loose and allow leakage or stay tight when you are trying to release urine.

Urine retention. For some people, nerve damage means their bladder muscles do not get the message that it is time to release urine or are too weak to completely empty the bladder. If the bladder becomes too full, urine may back up and the increasing pressure may damage the kidneys. Or urine that stays too long may lead to an infection in the kidneys or bladder. Urine retention may also lead to overflow incontinence.

What causes nerve damage?

Many events or conditions can damage nerves and nerve pathways. Some of the most common causes are

• vaginal childbirth
• infections of the brain or spinal cord
• diabetes
• stroke
• accidents that injure the brain or spinal cord
• multiple sclerosis
• heavy metal poisoning
• In addition, some children are born with nerve problems that can keep the bladder from releasing urine, leading to urinary infections or kidney damage.

How will the doctor test for nerve damage and bladder control problems?

Any evaluation for a health problem begins with a medical history and a general physical examination. Your doctor can use this information to narrow down the possible causes for your bladder problem.

If nerve damage is suspected, the doctor may need to test both the bladder itself and the nervous system, including the brain. Three different kinds of tests might be used:

Urodynamics. These tests involve measuring pressure in the bladder while it is being filled to see how much it can hold and then checking to see whether the bladder empties completely and efficiently.

Imaging. The doctor may use different types of equipment-x rays, magnetic resonance imaging (MRI), and computerized tomography (CT) scans-to take pictures of the urinary tract and nervous system, including the brain.

EEG and EMG. An electroencephalograph (EEG) is a test in which wires with pads are placed on the forehead to sense any dysfunction in the brain. The doctor may also use an electromyograph (EMG), which uses wires with pads placed on the lower abdomen to test the nerves and muscles of the bladder.

What are the treatments for overactive bladder?

The treatment for a bladder control problem depends on the cause of the nerve damage and the type of voiding dysfunction that results.

In the case of overactive bladder, your doctor may suggest a number of strategies, including bladder training, electrical stimulation, drug therapy, and, in severe cases where all other treatments have failed, surgery.

Bladder training. Your doctor may ask you to keep a bladder diary-a record of your fluid intake, trips to the bathroom, and episodes of urine leakage. This record may indicate a pattern and suggest ways to avoid accidents by making a point of using the bathroom at certain times of the day-a practice called timed voiding. As you gain control, you can extend the time between trips to the bathroom. Bladder training also includes Kegel exercises to strengthen the muscles that hold in urine.

Electrical stimulation. Mild electrical pulses can be used to stimulate the nerves that control the bladder and sphincter muscles. Depending on which nerves the doctor plans to treat, these pulses can be given through the vagina or anus, or by using patches on the skin. Another method is a minor surgical procedure to place the electric wire near the tailbone. This procedure involves two steps. First, the wire is placed under the skin and connected to a temporary stimulator, which you carry with you for several days. If your condition improves during this trial period, then the wire is placed next to the tailbone and attached to a permanent stimulator under your skin. The Food and Drug Administration (FDA) has approved this device, marketed as the InterStim system, to treat urge incontinence, urgency-frequency syndrome, and urinary retention in patients for whom other treatments have not worked.

A device can be placed under your skin to deliver mild electrical pulses to the nerves that control bladder function.

Drug therapy. Different drugs can affect the nerves and muscles of the urinary tract in different ways.

• Drugs that relax bladder muscles and prevent bladder spasms include oxybutynin chloride (Ditropan), tolterodine (Detrol), hyoscyamine (Levsin), and propantheline bromide (Pro-Banthine), which belong to the class of drugs called anticholinergics. Their most common side effect is dry mouth, although large doses may cause blurred vision, constipation, a faster heartbeat, and flushing. A new patch delivery system for oxybutynin (Oxytrol) may decrease side effects. Ditropan XL and Detrol LA are timed-release formulations that deliver a low level of the drug continuously in the body. These drugs have the advantage of once-a-day administration. In 2004, the FDA approved trospium chloride (Sanctura), darifenacin (Enablex), and solifenacin succinate (VESIcare) for the treatment of overactive bladder.
• Drugs for depression that also relax bladder muscles include imipramine hydrochloride (Tofranil), a tricyclic antidepressant. Side effects may include fatigue, dry mouth, dizziness, blurred vision, nausea, and insomnia.

Additional drugs are being evaluated for the treatment of overactive bladder and may soon receive FDA approval.

Surgery. In extreme cases, when incontinence is severe and other treatments have failed, surgery may be considered. The bladder may be made larger through an operation known as augmentation cystoplasty, in which a part of the diseased bladder is replaced with a section taken from the patient’s bowel. This operation may improve the ability to store urine but may make the bladder more difficult to empty, making regular catheterization necessary. Additional risks of surgery include the bladder breaking open and leaking urine into the body, bladder stones, mucus in the bladder, and infection.

How do you do Kegel exercises?

Kegel exercises strengthen the muscles that hold up the bladder and keep it closed.

The first step in doing Kegel exercises is to find the right muscles. Imagine you are trying to stop yourself from passing gas. Squeeze the muscles you would use. If you sense a “pulling” feeling, those are the right muscles for pelvic exercises.

Try not to squeeze other muscles at the same time. Be careful not to tighten your stomach, legs, or buttocks. Squeezing the wrong muscles can put more pressure on your bladder control muscles. Just squeeze the pelvic muscles. Don’t hold your breath.

At first, find a quiet spot to practice-your bathroom or bedroom-so you can concentrate. Pull in the pelvic muscles and hold for a count of 3. Then relax for a count of 3. Repeat, but don’t overdo it. Work up to 3 sets of 10 repeats. Start doing your pelvic muscle exercises lying down. This position is the easiest because the muscles do not need to work against gravity. When your muscles get stronger, do your exercises sitting or standing. Working against gravity is like adding more weight.

Be patient. Don’t give up. It takes just 5 minutes a day. You may not feel your bladder control improve for 3 to 6 weeks. Still, most people do notice an improvement after a few weeks.

Some people with nerve damage cannot tell whether they are doing Kegel exercises correctly. If you are not sure, ask your doctor or nurse to examine you while you try to do them. If you are not squeezing the right muscles, you can still learn proper Kegel exercises by doing special training with biofeedback, electrical stimulation, or both.

What are the treatments for lack of coordination between the bladder and urethra?

The job of the sphincter muscles is to hold urine in the bladder by squeezing the urethra shut. If the urethral sphincter fails to stay closed, urine may leak out of the bladder. When nerve signals are coordinated properly, the sphincter muscles relax to allow urine to pass through the urethra as the bladder contracts to push out urine. If the signals are not coordinated, the bladder and the sphincter may contract at the same time, so urine cannot pass easily.

Drug therapy for an uncoordinated bladder and urethra. Scientists have not yet found a drug that works selectively on the urethral sphincter muscles, but drugs used to reduce muscle spasms or tremors are sometimes used to help the sphincter relax. Baclofen (Lioresal) is prescribed for muscle spasms or cramping in patients with multiple sclerosis and spinal injuries. Diazepam (Valium) can be taken as a muscle relaxant or to reduce anxiety. Drugs called alpha-adrenergic blockers can also be used to relax the sphincter. Examples of these drugs are alfuzosin (UroXatral), tamsulosin (Flomax), terazosin (Hytrin), and doxazosin (Cardura). The main side effects are low blood pressure, dizziness, fainting, and nasal congestion. All of these drugs have been used to relax the urethral sphincter in people whose sphincter does not relax well on its own.

Botox injection. Botulinum toxin type A (Botox) is best known as a cosmetic treatment for facial wrinkles. Doctors have also found that botulinum toxin is useful in blocking spasms like eye ticks or relaxing muscles in patients with multiple sclerosis. Urologists have found that injecting botulinum toxin into the tissue surrounding the sphincter can help it to relax. Although the FDA has approved botulinum toxin only for facial cosmetic purposes, researchers are studying the safety and effectiveness of botulinum toxin injection into the sphincter for possible FDA approval in the future.

What are the treatments for urine retention?

Urine retention may occur either because the bladder wall muscles cannot contract or because the sphincter muscles cannot relax.

Catheter. A catheter is a thin tube that can be inserted through the urethra into the bladder to allow urine to flow into a collection bag. If you are able to place the catheter yourself, you can learn to carry out the procedure at regular intervals, a practice called clean intermittent catheterization. Some patients cannot place their own catheters because nerve damage affects their hand coordination as well as their voiding function. These patients need to have a caregiver place the catheter for them at regular intervals. If regular catheter placement is not feasible, the patients may need to have an indwelling catheter that can be changed less often. Indwelling catheters have several risks, including infection, bladder stones, and bladder tumors. However, if the bladder cannot be emptied any other way, then the catheter is the only way to stop the buildup of urine in the bladder that can damage the kidneys.

Urethral stent. Stents are small tube-like devices inserted into the urethra and allowed to expand, like a spring, widening the opening for urine to flow out. Stents can help prevent urine backup when the bladder wall and sphincter contract at the same time because of improper nerve signals. However, stents can cause problems if they move or lead to infection.

Surgery. Men may consider a surgery that removes the external sphincter-a sphincterotomy-or a piece of it-a sphincter resection-to prevent urinary retention. The surgeon will pass a thin instrument through the urethra to deliver electrical or laser energy that burns away sphincter tissue. Possible complications include bleeding that requires a transfusion and, rarely, problems with erections. This procedure causes loss of urine control and requires the patient to collect urine by wearing an external catheter that fits over the penis like a condom. No external collection device is available for women.

Urinary diversion. If other treatments fail and urine regularly backs up and damages the kidneys, the doctor may recommend a urinary diversion, a procedure that may require an outside collection bag attached to a stoma, a surgically created opening where urine passes out of the body. Another form of urinary diversion replaces the bladder with a continent urinary reservoir, an internal pouch made from sections of the bowel or other tissue. This method allows the person to store urine inside the body until a catheter is used to empty it through a stoma.

Hope through Research

The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) has many research programs aimed at fi nding treatments for urinary disorders, including bladder control problems caused by nerve damage. NIDDK-supported researchers have narrowed the search for a gene that causes neurological problems in bladder, bowel, and facial muscles. Finding the gene may lead to greater understanding of how nerves and muscles work together and how nerve damage can cause urination problems.

The Eunice Kennedy Shriver National Institute of Child Health and Human Development is supporting Collaborative Urological Research in Spinal Cord Injury, a program devoted to finding novel strategies to treat bladder control problems in people with spinal cord injury.

The U.S. Government does not endorse or favor any specific commercial product or company. Trade, proprietary, or company names appearing in this document are used only because they are considered necessary in the context of the information provided. If a product is not mentioned, the omission does not mean or imply that the product is unsatisfactory.

For More Information

American Urological Association Foundation
1000 Corporate Boulevard
Linthicum, MD 21090
Phone: 1-866-RING-AUA (746-4282) or 410-689-3700
Email: patienteducation@auafoundation.org
Internet: www.auafoundation.org
www.UrologyHealth.org

National Association for Continence
P.O. Box 1019
Charleston, SC 29402-1019
Phone: 1-800-BLADDER (252-3337) or 843-377-0900
Email: memberservices@nafc.org
Internet: www.nafc.org

You may also find additional information about this topic by visiting MedlinePlus at www.medlineplus.gov.

This publication may contain information about medications. When prepared, this publication included the most current information available. For updates or for questions about any medications, contact the U.S. Food and Drug Administration toll-free at 1-888-INFO-FDA (1-888-463-6332) or visit www.fda.gov. Consult your doctor for more information.

Source:  National Kidney and Urologic Diseases Information Clearinghouse

3 Information Way
Bethesda, MD 20892–3580
Phone: 1–800–891–5390
TTY: 1–866–569–1162
Fax: 703–738–4929
Email: nkudic@info.niddk.nih.gov
Internet: www.kidney.niddk.nih.gov

The National Kidney and Urologic Diseases Information Clearinghouse (NKUDIC) is a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). The NIDDK is part of the National Institutes of Health of the U.S. Department of Health and Human Services. Established in 1987, the Clearinghouse provides information about diseases of the kidneys and urologic system to people with kidney and urologic disorders and to their families, health care professionals, and the public. The NKUDIC answers inquiries, develops and distributes publications, and works closely with professional and patient organizations and Government agencies to coordinate resources about kidney and urologic diseases.

Comparing Two Modern Day Solutions For Cellulite Treatment: Liposuction V. Cellulite Reducers

 

 

By: Abbie Cheung

 

 

So what exactly is this evil cellulite that so many of us suffer from? Simply put, it is small amounts of fat that become trapped in pockets just below the skin’s surface. Because the fat is close to the surface, it creates the cottage cheese appearance we dislike so much.

Liposuction is an established way to get rid of cellulite, but now it is not the only option. New cellulite reducers have been developed which are safer, less invasive, and less expensive.

Long taken as the gold standard of cellulite reduction and elimination, liposuction is no longer the only option.

 
Liposuction works by removing fat deposits in a surgical procedure.

This surgery can cause scarring, swelling, infection, excess skin, and body contouring irregularities. Considering the high cost of liposuction and its possible side effects, non-invasive cellulite reducers start to look more and more appealing. If nothing else, it is at least safer to try these treatments before going for liposuction.

Cellulite reducers work by delivering active ingredients to cellulite-affected body parts and shrinking the cellulite.

Unlike liposuction, these treatments are not invasive and do not physically remove cellulite. One kind of cellulite reducers is pill-based. Cellulite-reducing pills work inside the body and for this reason may not be the most effective type of cellulite reducer. This is because the active ingredients can only work if they are able to effectively travel to and absorb into the target area. Body parts with a lot of cellulite tend to not have very good blood circulation and are therefore not as good at absorbing the active ingredients in cellulite reducers.

The other kind of cellulite reducers is cellulite creams.

Applied once or twice per day, these creams contain active ingredients designed to decrease the size of fat cells right under the skin. They give the skin more tone and smoothness, and they are usually quite moisturizing as well.

It makes sense to give a cellulite reducer a try.

These products do work. Most companies have many testimonials on their sites about successful clients, and these products also have no medical risks and will not hurt your pocketbook as much. In as little as 2 weeks some products will show an improvement, but you do need to be committed to the system. Remember nothing happens overnight. You need to follow the product instructions to ensure that you give the cellulite reducer time to do its job

Source: http://www.articlesnatch.com

Scientist: GM Food Safety Testing Is “Woefully Inadequate”

 

 

•     By Ken Roseboro
     

According to Judy Carman, Ph.D., very little safety testing is done on genetically modified foods, and when it is done, biotechnology companies conduct minimal testing. Dr. Carmen says that more extensive testing of GM foods is needed to ensure they are safe. Her recommendations seem prophetic in light of a recent Austrian government study that found reduced fertility in mice-fed GM corn.

Dr. Carmen is director of the Institute of Health and Environmental Research, Inc., a non=profit research institute based in Australia focusing on the safety of genetically modified food. She earned a doctorate degree in medicine from the University of Adelaide in the areas of metabolic regulation, nutritional biochemistry, and cancer. She has investigated outbreaks of disease for an Australian state government.

Ken Roseboro, editor of The Organic & Non-GMO Report, interviewed Dr. Judy Carmen during her recent visit to the United States.

Can you tell me about your research on the health impacts of GM foods?

We are conducting one the very few long-term, independent animal feeding studies with GM foods. To date, most of these types of studies have been done by biotechnology companies or scientists associated with biotechnology companies. Of the few independent studies being done, a study by the Austrian government recently made public found reduced fertility in mice fed GM corn. Another recent study done in Italy showed immune system problems in mice fed GM corn. The studies done by biotechnology companies tend to show no health problems associated with eating GM food. The independent studies are finding adverse effects.

Do you have any comments about the Austrian study showing reduced fertility?

I haven’t had a chance to read it yet. It is interesting that (Russian scientist) Irina Ermakova had similar findings (of reduced fertility) with mice fed GM soy. It is disturbing that the study showed a gradually worsening effect on mice that ate the GM corn. I am worried that something similar is happening in humans. If it is, it could take many years for problems to become apparent, and by then it could be too late to do anything about it.

What are the challenges of doing this type of research?

There are two major challenges. First, it is very hard to get GM seed to conduct the research. In order to buy GM seed, you have to go to a licensed seed dealer, and sign a technology licensing agreement, which states that you won’t do any research on the seed, which includes agronomic, health, and environmental research. Also, scientists who try to research health impacts of GM food get harassed and intimidated by people with vested interests in GM technology. I’ve had 10 years of abuse from such people who’ve defamed me, driven me out of a university, and tried to get me fired from jobs. With that kind of intimidation, scientists often decide not to do any research. Vested interests have been trying to find out about research I’m doing. They filed a freedom of information request with the Western Australian government to find out. The government denied their request. It could have ended up in court. My research protocol could have been stolen.

Funding for studied looking at health effects of GM foods is difficult to find in the United States. Do tyou find that universities and organizations in Australia also don’t want to fund such studies?

Yes, it is very difficult to get funding. If you want to do medical research, you have to go to an organization that funds such research. In order to get funding you need to have a proven track record in that area of research. However, in a new area of research such as GM food safety, no one has a track record, so it is difficult to get the funding. It’s a Catch-22. We are thankful that the Western Australian government gave us funding. The research protocol was sent to 15 scientists worldwide for review and then approved by a steering committee. I wanted people to know that I was doing a thorough job with this research.

If your research finds negative health impacts caused by GM foods, are you prepared to del with a negative onslaught from biotech companies?

Yes, I understand that will happen. I’ve been attacked many times. GM food advocates want to make people who do this type of work frightened of losing their jobs to make them stop working on the issue. They can’t get me fired now. I work within my own organization, the Institute of Health and Environmental Research, which I established along with others who are committed to finding out if GM foods are safe to eat. The behavior of GM food advocates makes me ask, “What are they frightened of?” If they believe GM foods are safe, they would be confident that I would not find any problems. Instead they are paranoid. What do they know that I don’t know? What are they trying to hide? It makes me more curious and determined to find out.

GM foods are widely consumed in the United States, and the US government opposed labeling GM foods. What are your thoughts about that?

The big surprise is the lack of GM food labeling here. In Australia, we hear all the time from the US that you are the land of the free. I find it amazing that Americans have no choice about eating GM foods. The most basic democratic right is being denied to you. For those who don’t want to eat GM food, it is being shoved down your throats against your will because it seems that nearly all foods have ingredients from GM corn or soy. With every US citizen exposed to GM foods, if something goes wrong it could go very badly wrong. If one person in a thousand gets sick from GM foods, that’s 300,000 people sick.

GM food advocates often claim that “no one in the US has ever gotten sick from eating GM foods.”

It’s rubbish to say that no one ever has ever gotten sick eating GM foods. The fact is that no one knows. Since GM foods have been introduced, millions of Americans have been hospitalized and millions have died, and no one has investigated to see if any of those cases have been due to eating GM foods. The HIV/AIDS epidemic went unnoticed for decades, and the relationship between smoking and lung cancer went undetected for generations. With the current level of safety testing, if GM foods do cause human health problems, it will be very difficult to determine this, even though there may be many cases of illness.

What type of safety testing do you think should be done on GM crops?

We need long-tern safety tests that are relevant to human health done by people independent of GM vested interests. The safety testing done now is woefully inadequate. Biotechnology companies often don’t even use the whole GM grain in feeding studies. Instead they tend to use only a protein extract that doesn’t even come from the GM plant. The feeding tests are also only done for few days or a few weeks. Safety tests should involve comparing animals fed GM foods with animals fed the equivalent non-GM food. The animals should be fed long enough and involve tests that, at a minimum, measure risks of cancer and allergy and threats to reproduction and organ health.

Do you believe that scientific research will conclusively show that GM foods pose significant health risks?

You never know what will happen. Independent research is finally being done and is showing adverse effects. There’s been an avalanche of bad news for the GM industry lately.

Source:

Organic Consumers Association · 6771 South Silver Hill Drive, Finland MN 55603

Is Your Shampoo Making You Fat?

 

This OnEarth column was written by Laura Fraser.

 

We all know that Americans — leading the way for the rest of the developed world — are getting fatter. We hear about the “obesity epidemic” on the TV news, with footage of people depicted from the waist down shuffling around in XXL sweatpants and carrying supersized sodas. The majority of us are overweight, complaining about how our jeans are getting tighter and wondering why, despite all our efforts to diet and go to the gym, the number on the scale keeps edging higher.

For years, the explanation for weight gain was straightforward: it was all about energy balance, or calories-in versus calories-out. This Gluttony and Sloth theory held that obesity simply came from overeating and under-exercising, and the only debate was about dieting — whether it was better to join the low-fat or the low-carb camp. Some scientists explored genetic differences associated with fat, but others said genes couldn’t possibly explain the rate at which Americans were gaining weight: “We just aren’t evolving that fast,” one obesity expert noted.

Environmental scientists have long suggested that there were likely external factors at work, but until recently, the traditional obesity-research community rejected such claims. Now it seems thatthe tide is turning: This month’s issue of Obesity Reviews features an extensive look at the accumulating body of research linking the environment with obesity.

The idea of our surroundings contributing to weight gain is nothing new, of course. But past discussions about the role of the “environment” focused mostly on the fast-food culture that we live in, where highly processed, highly caloric foods are constantly available, eating times are chaotic, kids run around drinking sugar-saturated sodas all day, no one has time to cook, fruits and vegetables are scarce in low-income urban areas, a venti frappuccino has 760 calories, and muffins are the size of melons. Add to that our changing physical environment — the fact that everyone sits in front of computers every day, instead of working out or working on the farm — and the “calories in” excess of the weight equation seems obvious, and obesity over-determined.

But even allowing for such influences, something wasn’t adding up. There are plenty of people out there who eat well and exercise like Gwyneth Paltrow and still feel like their weight is out of control. Then there are those annoying people who eat everything they desire, never work out, and stay thin. There had to be more to it than calories. We know that hormones — the chemical messengers produced by our endocrine system to control things like blood pressure and insulin production — can fatten up animals for slaughter; that some drugs increase your weight; and that a change in hormones at midlife shifts where your fat is distributed. Researchers began to recognize that obesity is much more complicated than calories in and out, and that a lot of other mechanisms involving the hormonal regulatory system are involved in our bodies’ delicate weight balance.

Paula Baillie-Hamilton, an expert on metabolism and environmental toxins at Stirling University in Scotland, was among the first to make the link between the obesity epidemic and the increase in the chemicals in our lives. “Overlooked in the obesity debate,” she wrote in 2002 in the Journal of Alternative and Complementary Medicine, “is that the earth’s environment has changed significantly during the last few decades because of the exponential production and usage of synthetic organic and inorganic chemicals.”

Exposure to those chemicals, said Baillie-Hamilton, can damage the body’s natural weight-control mechanisms. She calls toxic chemicals that act as endocrine disruptors — mimicking hormones, and blocking or exaggerating our natural hormonal responses — “chemical calories,” and those in question include Bisphenol A, phthalates, PCBs, persistent organic pollutants such as DDE, a breakdown product of the insecticide DDT, and pesticides containing tin compounds called organotins. Many studies have shown that endocrine disruptors have been linked to early puberty, impaired immune function, different types of cancer, birth deformities, and other diseases. Now obesity and metabolism are on that list.

Environmental researchers call these chemical calories “obesogens.” Bruce Blumberg, a University of California at Irvine professor of developmental and cell biology, studies the effects of endocrine disruptors on obesity in mice and sees clear differences between those who are exposed to them and those who aren’t. “Pretty much anyone who observes people knows that obesity is way more than eating and exercise,” says Blumberg. Instead, metabolism, appetite, and the number and size of fat cells you have come into play, all of which are affected by hormones, and therefore by hormone disruptors. Blumberg has shown that the organic pollutants tributyltin and triphenyltin derail the hormonal mechanisms that control the weight of mice. He’s found that when pregnant mice are fed a dose of organotins that is equivalent to normal human exposure to those chemicals, their offspring have 10 percent more fat cells than normal mice, the fat cells grow bigger than normal, and they end up, overall, 10 percent fatter than your average mouse.

Other compelling research that fat is not just about eating and exercise comes from studies that show that animals that live in human environments get fatter just by virtue of being around people. Researchers at the University of Alabama recently found that chimpanzees, macaques, mice, rats, dogs, cats, and other species that lived in proximity to humans got fatter than animals that didn’t live in an industrialized environment — even when their lab chow and exercise was highly controlled. The authors suggested that endocrine disruptors were one likely culprit in this cross-species obesity epidemic.

For her article in the new Obesity Reviews, Jeanett Tang-Peronard, of the Institute of Preventive Medicine in Copenhagen, looked at some 450 studies on endocrine disruptors and obesity and found that nearly all of them showed a correlation between exposure to those chemicals — particularly in utero and in early childhood, when hormonal mechanisms are vulnerable — and an increase in body size. She says that in early life, chemicals seem to alter the epigenetic regulation of certain genes, disrupting the programming of hormonal signaling pathways that affect fat storage, fat distribution, and appetite. (The epigenome governs patterns of gene expression.) This reprogramming could explain how we are indeed evolving so fast.

Tang-Peronard says that it is impossible, now, to tease out how much of obesity is caused by chemicals, and how much by energy balance. They’re intertwined, anyway, with imbalances in appetite-regulating hormones like leptin and ghrelin causing us to want to eat more of the available food. “Endocrine disruptors may play a significant role in obesity,” she says. But the research is in its infancy. She also points out that only a few of the tens of thousands of known environmental chemicals have been tested for their association with obesity. “We are only scratching the surface,” she says.

What to do about the problem of endocrine disruptors and obesity? It’s hard to say, given that virtually all humans have been exposed. Pediatrician Maida Galvez is involved in the Mt. Sinai “Growing Up Healthy“ study of 330 children in East Harlem, monitoring their exposure to endocrine disruptors and their body weight. “Even if these chemicals play a small role in obesity, it’s a preventable exposure,” she says, explaining that if certain substances can be determined to have deleterious effects, we can avoid them at critical stages of development and ultimately replace them with safer alternatives.

For now, Galvez recommends that parents steer clear of Bisphenol-A — present in many plastic water and baby bottles, and in microwavable and dishwasher-safe food containers. (If you find a printed “7″ on the bottom, get rid of it.) She also suggests avoiding shampoos, cosmetics, and soaps containing phthalates — up to 70 percent of “top-selling products,” according to a 2002 report by the Environmental Working Group. (Look for fragrance-free products, which are less likely to contain phthalates, or for anything from the Illumina Organics range or The Body Shop. And, she says, eat fresh fruits and vegetables, instead of foods that are processed and/or packaged in plastic.

That’s one point on which traditional obesity researchers and environmental scientists agree: Eat plenty of fresh, organic vegetables. And while you’re at it, get out into the fresh air and get some exercise.

Featuring great stories and great solutions, OnEarth magazine is a survival guide for the planet.

Source: Organic Consumers Association (OCA)/ OnEarth Magazine

Are You Addicted To Food?

 

By Rachael Moeller Gorman, “Addicted to Food?,”March/April 2011 in Eating Well

Food can enslave the brain just like drugs can. Dr. Nora Volkow’s research may help you take back control.

Every morning, Nora Volkow walks past a vending machine on her way to her office. She barely notices it. One day, however, she’s hungry, so she stops and peers in. A chocolate bar grabs her eye. She inserts her money, takes the chocolate, munches, and moves on. The next day, Volkow walks to her office as usual, but this time as she rounds the corner, she has a sudden, intense craving for chocolate. She hadn’t thought about it since her last bite the day before. She isn’t hungry. “But my brain responded in this automatic way,” she explains in her melodic Spanish accent as she sits in her office at the National Institute on Drug Abuse (NIDA), where she serves as director. Because the chocolate had given her so much enjoyment, just the sight of the machine made her want to eat more.

Volkow, a lithe woman with short blonde curls, provides example after example of instances in which she has succumbed to the food’s lure. Chocolate-covered raisins. Godiva at a bookstore. Chocolate-chip cookies. The woman really, really likes chocolate.

But is she an addict? People talk about being “addicted to sugar,” “addicted to potato chips” and, probably most commonly, “addicted to chocolate.” Volkow has been attempting to figure out whether we truly can be addicted to food by peering into people’s minds with high-tech scanners. She has already shown that obese people’s brains look similar to the brains of those addicted to drugs. She’s finding that food, especially the highly palatable fatty, sugary kinds that pack the inner aisles of American supermarkets, fast-food joints and, yes, vending machines, can enslave anyone and change their behaviors.

The more she can understand how “rewarding” substances, like drugs and yummy foods, can activate parts of our brains associated with addiction, the more she can help us learn how to take back control of our actions—or never lose our free will in the first place.

The Makings of a Pioneer

If you were to imagine a person whose pedigree and character destines her for a key leadership role, an NIH director, say, you might picture someone quite like Nora Volkow. Volkow’s great-grandfather was Leon Trotsky, the famous Russian revolutionary who defied Stalin, only to later be murdered in exile in Volkow’s childhood home in Mexico City. Her mother, a Spanish fashion designer, died several years ago, and her father is a chemist who still lives in Mexico. Nora Volkow herself graduated first in her class at the National University of Mexico medical school and received the Premio Robins award for best medical student of her generation. She speaks four languages fluently. She runs seven miles before work every day. She works an average of 80 hours every week.

Yet for the sake of science, she perpetually brings up her own weaknesses. Like chocolate. Which we keep coming back to.

“The other day someone gave me chocolate-covered raisins,” she says, swinging her ID chain with both hands, a twinkle in her eye. “They gave me two boxes, so I say, OK, I’ll eat half a box. Well, I ate one-and-a-half boxes!” This sort of compulsive eating, she says, is one reason that obesity has become an epidemic. Many people blame obese people for their condition, saying they simply eat too much. But it’s not that obese people lack willpower, says Volkow; there is something physical happening in their brains that prevents them from stopping. “Obesity is highly, horrifically stigmatized,” says Volkow. “It erodes your self-esteem, it interferes with social interactions, it affects your mobility. And yet so often people cannot stop it.”

The Dopamine Made Me Do It

Volkow’s interest in the chemistry and mechanisms of the brain began in Mexico City in 1981. She had just graduated from medical school and read an article in Scientific American about exciting new clinical applications of a technology called positron emission tomography (PET). PET allows scientists to see a three-dimensional image of the brain as it thinks, feels and works (previously, scientists could not watch the brain in action very well). Volkow was awestruck, and applied for a psychiatric residency at New York University to have a chance to work with nearby PET pioneers at the Department of Energy’s Brookhaven National Laboratory on Long Island.

She was particularly interested in the brains of people who lose the ability to control their actions rationally; people who, in essence, lose free will. At first, she studied schizophrenics. By the late 1980s, she started looking at the brains of alcoholics and drug addicts as well. She soon saw that the addicted brains looked decidedly different from brains of people without drug or alcohol addictions.

The most marked difference was in the dopamine cells of the reward circuit, a group of brain cells that communicate using the chemical dopamine. The circuit connects several regions in the brain involved in the feeling of reward, which has evolved to motivate us to do more of the things that make us feel good and are important for survival, like eating, having sex and taking care of children. Drugs like cocaine and amphetamines highjack this circuit, causing a flood of dopamine into the area between brain cells where messages are transmitted. And this dopamine surge produces a high. Take the drugs often enough and dopamine receptors can decrease in number or become less sensitive to dopamine. When this happens, a person needs more and more of the drug to get the same effect (this is called tolerance).

As a psychiatrist, Volkow noted a similarity between drug abusers and compulsive overeaters: they both seemed to lose their rational ability to control their behaviors (around drugs and food, respectively). She wanted to know how to intervene to help those who couldn’t stop themselves. She knew that antipsychotic drugs, which block the reward-registering dopamine system, often make people eat and gain weight (as a side effect), while drugs that increase dopamine in the brain cause weight loss. In 2001, Volkow and her colleagues began exploring whether dopamine played a key role in overeating and obesity in people not on drugs.

To find out, Volkow and her crew gave a radioactive chemical that binds to dopamine receptors to 20 people—10 obese, 10 normal weight—and then scanned their brains using PET, to see whether there were any associations between their dopamine systems and their body weights.

Turns out, there were. The obese people had significantly fewer dopamine receptors in a part of the brain called the striatum. Volkow and her team surmised that with fewer receptors, the people who were obese had to eat far more food than a normal-weight person to experience the same high.

Liking and Wanting

In 2002, Volkow published a study that investigated the link between dopamine and “wanting.” When people were presented with—but not allowed to eat—warm, tasty plates of their favorite food, dopamine increased in the striatum area of their brains. The subjects said they were hungry and desired the food. This is the “wanting,” or craving; it is not the pleasure (i.e., “liking”) they likely would have experienced if they had been allowed to consume it. The people’s responses in this study were quite similar to the experiences of drug abusers watching a video showing people using cocaine: the abusers experience a dopamine surge through the parts of the brain involved in habit.

In other words, really liking chocolate or potato chips, the pleasure that occurs when your reward systems fire, isn’t the whole story of dopamine and addiction. An intense want—the desire to eat, to do everything you can to get your hands on a food and put it into your mouth—is equally important. You taste creamy milk chocolate or a salty French fry. You really, really like it. So much so that you’re conditioned to the setting in which you ate the yummy food and the next time you’re in that environment, a shot of dopamine squirts into your brain and you want that food. You crave it. You’re motivated to eat it—and to keep eating it.

This idea is central to the obesity epidemic. “There is a certain reinforcement, almost like an arousal of wanting more,” says Volkow. “A person eats a gallon of ice cream. He is not even realizing the taste of the food anymore, he’s not enjoying the pleasure of the palatability and experience; it has become automatic. The drive to have more and more [fueled by dopamine] is what maintains that behavior, independent at that point of the pleasurable response that you get.

“It’s almost like they become a robot.”

You’ve Been Conditioned

No one would become a food-devouring robot, however, if they lived in a desert or on the moon or in the year 1850, according to David Kessler, M.D., former FDA commissioner and author of The End of Overeating (Rodale, 2009). We eat, he says, because we have constant, crippling access to rich, delicious foods packed with fat and sugars, both of which activate our dopamine systems. And those conditioned cues are everywhere—commercials, fast-food restaurants that we pass on our commutes, grocery stores. Kessler postulates that fat and sugar, plus salt, have triggered mass overconsumption in the United States.

“We took fat, sugar and salt and put it on every corner, made it available 24/7, made it socially acceptable to eat anytime. We’re living in a food carnival,” he says.

Volkow’s Bethesda offices are a perfect microcosm of this American food environment: Within one-third of a mile, a visitor can find a frozen yogurt place, a greasy-spoon diner, a Mexican restaurant and at least 10 other eateries. On the first floor of the NIDA offices is a cafeteria with a hot buffet and snacks. Vending machines, like the one Volkow has a hard time resisting, live on the office floors themselves. Bowls of candy lurk on desktops and in drawers. The scent of microwave popcorn pervades the office air.

The continual need to say “NO!” to these tempting foods requires the strongest will, and some people’s wiring seems to be working against them. In a 2008 study, Volkow found that having fewer dopamine receptors (as obese people do) was associated with less activity in parts of the brain responsible for self-control. In other words, these people not only have to eat more to achieve the same “reward,” they also have a harder time stopping themselves from eating once they start. Drug addicts similarly have fewer dopamine receptors, also associated with less activity in the self-control parts of the brain. In the brain of a compulsive, “addicted” eater, inhibition is like a picket fence trying to hold back an avalanche of reward and conditioning.

“Joanne,” 39, from San Francisco, a member of Food Addicts in Recovery Anonymous, agrees, and says that sugar and flour are her drugs. Since she was a teenager, Joanne would compulsively eat for hours at a time; in high school she learned how to make herself sick, which “led to 15 years of insanity,” she says. “There was something in my brain that would light up, and it would turn into this massive craving that I could not control.”

Joanne’s food addiction manifested as bulimia, but others in the group became obese. When she wasn’t purging, she was “white-knuckling it” through the day. “If there was food somewhere in the vicinity, the constant conversation in my head was, ‘Should I eat that? No, don’t eat that.’ Back and forth, over and over, while trying to maintain a conversation, which was almost fruitless because I wasn’t really listening, I was focused on the food.” Studies have estimated that about 10 percent of the population is addicted to food like this, and many more of us probably fall elsewhere on the food-addiction spectrum.

“Everyone understands how critical taste is [to overeating], but what Nora has shown is the role not just of taste, but of the brain and brain circuits,” says Kessler. “We now know that the learning, memory, habit and motivational circuits of the brain are what drive eating, and Nora deserves a lot of credit for pulling back the curtain and showing us what’s really at the core of this [obesity] epidemic.”

Breaking the Cycle

But even though we are inundated with hyper-palatable food, not everyone becomes an addict. “At least 50 percent of that vulnerability is related to genetics,” Volkow says. And your ability to put on the brakes is a crucial factor. “Some people are [naturally] much better at controlling their desires than others.” After genetics, Volkow says the rest is environment—if you only have access to high-calorie, cheap junk foods, that’s all you can eat.

Not everyone in the field agrees that people can be addicted to food and they object to the excuse it provides. “Interest in obesity as a brain disease should not detract from a public health focus on the ‘toxic food environment’ that is arguably responsible for the obesity epidemic,” writes psychologist Terry Wilson, Ph.D., of Rutgers University in a 2010 paper. But those who study food addiction say it does bear striking similarity to drug and alcohol addition: Ashley Gearhardt, Kelly Brownell and William Corbin at Yale have created the Yale Food Addiction Scale to determine whether a person is truly addicted to food. They adapted it from the scale for substance dependence in the DSM-IV (the “Bible” of psychiatry), and it includes criteria like whether the subject has been unsuccessful in trying to quit, whether he or she spends a lot of time trying to obtain the food, whether he or she has given up other recreational activities for the food, whether there are adverse consequences of eating the food, whether the subject becomes tolerant to the food and whether they have withdrawal symptoms. When they surveyed 233 people, these three leading researchers found that 11.6 percent of them could be diagnosed with food dependence (consuming large amounts of food despite significant issues—obesity, health problems—associated with it and the desire to stop, as well as withdrawal or tolerance). The scale could be useful in determining treatment for addicts versus those who simply experience the occasional craving.

Back in her office, surrounded by sculptures and paintings, some from her own hand (yes, she’s an artist too!), Volkow talks about how addiction steals our free will and makes us a slave to the salient substance. So is Nora Volkow a chocolate addict? “No, I’m not. We use the word way too much.” The distinction, she says, is when eating the food impairs your life, when you lose control, like when a person consistently eats so much they only eat in private out of embarrassment and spend much of their time thinking about food. “Most people [who] take drugs are not addicted to drugs, like most people who eat chocolate, even if they eat more than they should, are not addicted to chocolate.

“I may have that vulnerability, perhaps, for compulsiveness, but I am lucky enough to also have the control that leads me to plan ahead and say, I’m not going to do these things.” In other words, you can extend a hand from a present moment of strength to a future instance of weakness and wrestle your free will back from the dopamine master within.

Source: Rachael Moeller Gorman, an award-winning science writer, is a contributing editor for EatingWell.

About the Author:

An award-winning journalist, Rachael Moeller Gorman is a contributing editor at EatingWell and has written for such publications as Scientific American, Good Housekeeping, Discover, Proto, Cooking Light and The Boston Globe Health/Science section, among others. She loves learning about all things science, from the environment to anthropology to medicine, and enjoys translating dense jargon into elegant prose for a variety of audiences. Profiles are her favorite, and traveling to a research site for a story is always ideal.

Rachael has her bachelor’s degree in biology and neuroscience from Williams College and a master’s degree in environmental studies from Brown University. She has also conducted research in various genetics and neuroscience laboratories and is a member of the American Society of Journalists and Authors and the National Association of Science Writers. Please see the Articles section for a selection of her work.

Relationship Between Diabetes and Acne

 

By Pauline Go

In present times, nearly 85 percent people all over the world carry on a daily battle with acne and many of these people get it because acne is linked with many other problems and diseases. Research has been conducted as to why people get acne but until now no cause has been found, but most dermatologist agree that acne is caused due to hormonal imbalance.

Many people with diabetes also suffer from acne and they would like to know whether there is a link between diabetes and acne. However, there seems to be no consensus in the scientific world and there is controversy surrounding the link between diabetes and acne.

If a person suffers from acne and the pustules show little or no sign of healing, or they tend to reappear over and over again, many people think that it may be a sign of diabetes. This is because the first sign of diabetes is poor wound healing ability of the body. So, if you are over 40 and suffer from acne, there is a high possibility that you have diabetes.

In fact, you might be surprised to hear that Type II diabetes has acne as one of the symptoms. Usually in this type of acne, the acne pustules are painful and do not heal easily. Unfortunately many people suffering from diabetes do not notice acne symptoms. They pay more attention to frequent thirst and urination. However, if you have all the three symptoms, it is best to get your blood glucose level checked.

If you are diagnosed with diabetes, you can be sure that the acne will disappear once your start receiving treatment for diabetes. It is important that you learn not your scratch or burst the acne or it will aggravate your condition further.

Even with this, the link between diabetes ad acne is not very clear. According to some scientists, the excess insulin in the body causes the male hormone levels to increase and this in turn causes the acne. However, other scientists do not agree with this theory.

About Author:
Pauline Go is an online leading expert in medical industry. She also offers top quality medical tips like:
Facts About The Mosquito, Male Baldness Organin

Article Source: http://EzineArticles.com/?expert=Pauline_Go

Is Sugar Toxic ?

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April 13, 2011

Is Sugar Toxic?

By GARY TAUBES 

On May 26, 2009, Robert Lustig gave a lecture called “Sugar: The Bitter Truth,” which was posted on YouTube the following July. Since then, it has been viewed well over 800,000 times, gaining new viewers at a rate of about 50,000 per month, fairly remarkable numbers for a 90-minute discussion of the nuances of fructose biochemistry and human physiology.

Lustig is a specialist on pediatric hormone disorders and the leading expert in childhood obesity at the University of California, San Francisco, School of Medicine, which is one of the best medical schools in the country. He published his first paper on childhood obesity a dozen years ago, and he has been treating patients and doing research on the disorder ever since.

The viral success of his lecture, though, has little to do with Lustig’s impressive credentials and far more with the persuasive case he makes that sugar is a “toxin” or a “poison,” terms he uses together 13 times through the course of the lecture, in addition to the five references to sugar as merely “evil.” And by “sugar,” Lustig means not only the white granulated stuff that we put in coffee and sprinkle on cereal — technically known as sucrose — but also high-fructose corn syrup, which has already become without Lustig’s help what he calls “the most demonized additive known to man.”

It doesn’t hurt Lustig’s cause that he is a compelling public speaker. His critics argue that what makes him compelling is his practice of taking suggestive evidence and insisting that it’s incontrovertible. Lustig certainly doesn’t dabble in shades of gray. Sugar is not just an empty calorie, he says; its effect on us is much more insidious. “It’s not about the calories,” he says. “It has nothing to do with the calories. It’s a poison by itself.”

If Lustig is right, then our excessive consumption of sugar is the primary reason that the numbers of obese and diabetic Americans have skyrocketed in the past 30 years. But his argument implies more than that. If Lustig is right, it would mean that sugar is also the likely dietary cause of several other chronic ailments widely considered to be diseases of Western lifestyles — heart disease, hypertension and many common cancers among them.

The number of viewers Lustig has attracted suggests that people are paying attention to his argument. When I set out to interview public health authorities and researchers for this article, they would often initiate the interview with some variation of the comment “surely you’ve spoken to Robert Lustig,” not because Lustig has done any of the key research on sugar himself, which he hasn’t, but because he’s willing to insist publicly and unambiguously, when most researchers are not, that sugar is a toxic substance that people abuse. In Lustig’s view, sugar should be thought of, like cigarettes and alcohol, as something that’s killing us.

This brings us to the salient question: Can sugar possibly be as bad as Lustig says it is?

It’s one thing to suggest, as most nutritionists will, that a healthful diet includes more fruits and vegetables, and maybe less fat, red meat and salt, or less of everything. It’s entirely different to claim that one particularly cherished aspect of our diet might not just be an unhealthful indulgence but actually be toxic, that when you bake your children a birthday cake or give them lemonade on a hot summer day, you may be doing them more harm than good, despite all the love that goes with it. Suggesting that sugar might kill us is what zealots do. But Lustig, who has genuine expertise, has accumulated and synthesized a mass of evidence, which he finds compelling enough to convict sugar. His critics consider that evidence insufficient, but there’s no way to know who might be right, or what must be done to find out, without discussing it.

If I didn’t buy this argument myself, I wouldn’t be writing about it here. And I also have a disclaimer to acknowledge. I’ve spent much of the last decade doing journalistic research on diet and chronic disease — some of the more contrarian findings, on dietary fat, appeared in this magazine —– and I have come to conclusions similar to Lustig’s.

The history of the debate over the health effects of sugar has gone on far longer than you might imagine. It is littered with erroneous statements and conclusions because even the supposed authorities had no true understanding of what they were talking about. They didn’t know, quite literally, what they meant by the word “sugar” and therefore what the implications were.

So let’s start by clarifying a few issues, beginning with Lustig’s use of the word “sugar” to mean both sucrose — beet and cane sugar, whether white or brown — and high-fructose corn syrup. This is a critical point, particularly because high-fructose corn syrup has indeed become “the flashpoint for everybody’s distrust of processed foods,” says Marion Nestle, a New York University nutritionist and the author of “Food Politics.”

This development is recent and borders on humorous. In the early 1980s, high-fructose corn syrup replaced sugar in sodas and other products in part because refined sugar then had the reputation as a generally noxious nutrient. (“Villain in Disguise?” asked a headline in this paper in 1977, before answering in the affirmative.) High-fructose corn syrup was portrayed by the food industry as a healthful alternative, and that’s how the public perceived it. It was also cheaper than sugar, which didn’t hurt its commercial prospects. Now the tide is rolling the other way, and refined sugar is making a commercial comeback as the supposedly healthful alternative to this noxious corn-syrup stuff. “Industry after industry is replacing their product with sucrose and advertising it as such — ‘No High-Fructose Corn Syrup,’ ” Nestle notes.

But marketing aside, the two sweeteners are effectively identical in their biological effects. “High-fructose corn syrup, sugar — no difference,” is how Lustig put it in a lecture that I attended in San Francisco last December. “The point is they’re each bad — equally bad, equally poisonous.”

Refined sugar (that is, sucrose) is made up of a molecule of the carbohydrate glucose, bonded to a molecule of the carbohydrate fructose — a 50-50 mixture of the two. The fructose, which is almost twice as sweet as glucose, is what distinguishes sugar from other carbohydrate-rich foods like bread or potatoes that break down upon digestion to glucose alone. The more fructose in a substance, the sweeter it will be. High-fructose corn syrup, as it is most commonly consumed, is 55 percent fructose, and the remaining 45 percent is nearly all glucose. It was first marketed in the late 1970s and was created to be indistinguishable from refined sugar when used in soft drinks. Because each of these sugars ends up as glucose and fructose in our guts, our bodies react the same way to both, and the physiological effects are identical. In a 2010 review of the relevant science, Luc Tappy, a researcher at the University of Lausanne in Switzerland who is considered by biochemists who study fructose to be the world’s foremost authority on the subject, said there was “not the single hint” that H.F.C.S. was more deleterious than other sources of sugar.

The question, then, isn’t whether high-fructose corn syrup is worse than sugar; it’s what do they do to us, and how do they do it? The conventional wisdom has long been that the worst that can be said about sugars of any kind is that they cause tooth decay and represent “empty calories” that we eat in excess because they taste so good.

By this logic, sugar-sweetened beverages (or H.F.C.S.-sweetened beverages, as the Sugar Association prefers they are called) are bad for us not because there’s anything particularly toxic about the sugar they contain but just because people consume too many of them.

Those organizations that now advise us to cut down on our sugar consumption — the Department of Agriculture, for instance, in its recent Dietary Guidelines for Americans, or the American Heart Association in guidelines released in September 2009 (of which Lustig was a co-author) — do so for this reason. Refined sugar and H.F.C.S. don’t come with any protein, vitamins, minerals, antioxidants or fiber, and so they either displace other more nutritious elements of our diet or are eaten over and above what we need to sustain our weight, and this is why we get fatter.

Whether the empty-calories argument is true, it’s certainly convenient. It allows everyone to assign blame for obesity and, by extension, diabetes — two conditions so intimately linked that some authorities have taken to calling them “diabesity” — to overeating of all foods, or underexercising, because a calorie is a calorie. “This isn’t about demonizing any industry,” as Michelle Obama said about her Let’s Move program to combat the epidemic of childhood obesity. Instead it’s about getting us — or our children — to move more and eat less, reduce our portion sizes, cut back on snacks.

Lustig’s argument, however, is not about the consumption of empty calories — and biochemists have made the same case previously, though not so publicly. It is that sugar has unique characteristics, specifically in the way the human body metabolizes the fructose in it, that may make it singularly harmful, at least if consumed in sufficient quantities.

The phrase Lustig uses when he describes this concept is “isocaloric but not isometabolic.” This means we can eat 100 calories of glucose (from a potato or bread or other starch) or 100 calories of sugar (half glucose and half fructose), and they will be metabolized differently and have a different effect on the body. The calories are the same, but the metabolic consequences are quite different.

The fructose component of sugar and H.F.C.S. is metabolized primarily by the liver, while the glucose from sugar and starches is metabolized by every cell in the body. Consuming sugar (fructose and glucose) means more work for the liver than if you consumed the same number of calories of starch (glucose). And if you take that sugar in liquid form — soda or fruit juices — the fructose and glucose will hit the liver more quickly than if you consume them, say, in an apple (or several apples, to get what researchers would call the equivalent dose of sugar). The speed with which the liver has to do its work will also affect how it metabolizes the fructose and glucose.

In animals, or at least in laboratory rats and mice, it’s clear that if the fructose hits the liver in sufficient quantity and with sufficient speed, the liver will convert much of it to fat. This apparently induces a condition known as insulin resistance, which is now considered the fundamental problem in obesity, and the underlying defect in heart disease and in the type of diabetes, type 2, that is common to obese and overweight individuals. It might also be the underlying defect in many cancers.

If what happens in laboratory rodents also happens in humans, and if we are eating enough sugar to make it happen, then we are in trouble.

The last time an agency of the federal government looked into the question of sugar and health in any detail was in 2005, in a report by the Institute of Medicine, a branch of the National Academies. The authors of the report acknowledged that plenty of evidence suggested that sugar could increase the risk of heart disease and diabetes — even raising LDL cholesterol, known as the “bad cholesterol”—– but did not consider the research to be definitive. There was enough ambiguity, they concluded, that they couldn’t even set an upper limit on how much sugar constitutes too much. Referring back to the 2005 report, an Institute of Medicine report released last fall reiterated, “There is a lack of scientific agreement about the amount of sugars that can be consumed in a healthy diet.” This was the same conclusion that the Food and Drug Administration came to when it last assessed the sugar question, back in 1986. The F.D.A. report was perceived as an exoneration of sugar, and that perception influenced the treatment of sugar in the landmark reports on diet and health that came after.

The Sugar Association and the Corn Refiners Association have also portrayed the 1986 F.D.A. report as clearing sugar of nutritional crimes, but what it concluded was actually something else entirely. To be precise, the F.D.A. reviewers said that other than its contribution to calories, “no conclusive evidence on sugars demonstrates a hazard to the general public when sugars are consumed at the levels that are now current.” This is another way of saying that the evidence by no means refuted the kinds of claims that Lustig is making now and other researchers were making then, just that it wasn’t definitive or unambiguous.

What we have to keep in mind, says Walter Glinsmann, the F.D.A. administrator who was the primary author on the 1986 report and who now is an adviser to the Corn Refiners Association, is that sugar and high-fructose corn syrup might be toxic, as Lustig argues, but so might any substance if it’s consumed in ways or in quantities that are unnatural for humans. The question is always at what dose does a substance go from being harmless to harmful? How much do we have to consume before this happens?

When Glinsmann and his F.D.A. co-authors decided no conclusive evidence demonstrated harm at the levels of sugar then being consumed, they estimated those levels at 40 pounds per person per year beyond what we might get naturally in fruits and vegetables — 40 pounds per person per year of “added sugars” as nutritionists now call them. This is 200 calories per day of sugar, which is less than the amount in a can and a half of Coca-Cola or two cups of apple juice. If that’s indeed all we consume, most nutritionists today would be delighted, including Lustig.

But 40 pounds per year happened to be 35 pounds less than what Department of Agriculture analysts said we were consuming at the time — 75 pounds per person per year — and the U.S.D.A. estimates are typically considered to be the most reliable. By the early 2000s, according to the U.S.D.A., we had increased our consumption to more than 90 pounds per person per year.

That this increase happened to coincide with the current epidemics of obesity and diabetes is one reason that it’s tempting to blame sugars — sucrose and high-fructose corn syrup — for the problem. In 1980, roughly one in seven Americans was obese, and almost six million were diabetic, and the obesity rates, at least, hadn’t changed significantly in the 20 years previously. By the early 2000s, when sugar consumption peaked, one in every three Americans was obese, and 14 million were diabetic.

This correlation between sugar consumption and diabetes is what defense attorneys call circumstantial evidence. It’s more compelling than it otherwise might be, though, because the last time sugar consumption jumped markedly in this country, it was also associated with a diabetes epidemic.

In the early 20th century, many of the leading authorities on diabetes in North America and Europe (including Frederick Banting, who shared the 1923 Nobel Prize for the discovery of insulin) suspected that sugar causes diabetes based on the observation that the disease was rare in populations that didn’t consume refined sugar and widespread in those that did. In 1924, Haven Emerson, director of the institute of public health at Columbia University, reported that diabetes deaths in New York City had increased as much as 15-fold since the Civil War years, and that deaths increased as much as fourfold in some U.S. cities between 1900 and 1920 alone. This coincided, he noted, with an equally significant increase in sugar consumption — almost doubling from 1890 to the early 1920s — with the birth and subsequent growth of the candy and soft-drink industries.

Emerson’s argument was countered by Elliott Joslin, a leading authority on diabetes, and Joslin won out. But his argument was fundamentally flawed. Simply put, it went like this: The Japanese eat lots of rice, and Japanese diabetics are few and far between; rice is mostly carbohydrate, which suggests that sugar, also a carbohydrate, does not cause diabetes. But sugar and rice are not identical merely because they’re both carbohydrates. Joslin could not know at the time that the fructose content of sugar affects how we metabolize it.

Joslin was also unaware that the Japanese ate little sugar. In the early 1960s, the Japanese were eating as little sugar as Americans were a century earlier, maybe less, which means that the Japanese experience could have been used to support the idea that sugar causes diabetes. Still, with Joslin arguing in edition after edition of his seminal textbook that sugar played no role in diabetes, it eventually took on the aura of undisputed truth.

Until Lustig came along, the last time an academic forcefully put forward the sugar-as-toxin thesis was in the 1970s, when John Yudkin, a leading authority on nutrition in the United Kingdom, published a polemic on sugar called “Sweet and Dangerous.” Through the 1960s Yudkin did a series of experiments feeding sugar and starch to rodents, chickens, rabbits, pigs and college students. He found that the sugar invariably raised blood levels of triglycerides (a technical term for fat), which was then, as now, considered a risk factor for heart disease. Sugar also raised insulin levels in Yudkin’s experiments, which linked sugar directly to type 2 diabetes. Few in the medical community took Yudkin’s ideas seriously, largely because he was also arguing that dietary fat and saturated fat were harmless. This set Yudkin’s sugar hypothesis directly against the growing acceptance of the idea, prominent to this day, that dietary fat was the cause of heart disease, a notion championed by the University of Minnesota nutritionist Ancel Keys.

A common assumption at the time was that if one hypothesis was right, then the other was most likely wrong. Either fat caused heart disease by raising cholesterol, or sugar did by raising triglycerides. “The theory that diets high in sugar are an important cause of atherosclerosis and heart disease does not have wide support among experts in the field, who say that fats and cholesterol are the more likely culprits,” as Jane E. Brody wrote in The Times in 1977.

At the time, many of the key observations cited to argue that dietary fat caused heart disease actually support the sugar theory as well. During the Korean War, pathologists doing autopsies on American soldiers killed in battle noticed that many had significant plaques in their arteries, even those who were still teenagers, while the Koreans killed in battle did not. The atherosclerotic plaques in the Americans were attributed to the fact that they ate high-fat diets and the Koreans ate low-fat. But the Americans were also eating high-sugar diets, while the Koreans, like the Japanese, were not.

In 1970, Keys published the results of a landmark study in nutrition known as the Seven Countries Study. Its results were perceived by the medical community and the wider public as compelling evidence that saturated-fat consumption is the best dietary predictor of heart disease. But sugar consumption in the seven countries studied was almost equally predictive. So it was possible that Yudkin was right, and Keys was wrong, or that they could both be right. The evidence has always been able to go either way.

European clinicians tended to side with Yudkin; Americans with Keys. The situation wasn’t helped, as one of Yudkin’s colleagues later told me, by the fact that “there was quite a bit of loathing” between the two nutritionists themselves. In 1971, Keys published an article attacking Yudkin and describing his evidence against sugar as “flimsy indeed.” He treated Yudkin as a figure of scorn, and Yudkin never managed to shake the portrayal.

By the end of the 1970s, any scientist who studied the potentially deleterious effects of sugar in the diet, according to Sheldon Reiser, who did just that at the U.S.D.A.’s Carbohydrate Nutrition Laboratory in Beltsville, Md., and talked about it publicly, was endangering his reputation. “Yudkin was so discredited,” Reiser said to me. “He was ridiculed in a way. And anybody else who said something bad about sucrose, they’d say, ‘He’s just like Yudkin.’ ”

What has changed since then, other than Americans getting fatter and more diabetic? It wasn’t so much that researchers learned anything particularly new about the effects of sugar or high-fructose corn syrup in the human body. Rather the context of the science changed: physicians and medical authorities came to accept the idea that a condition known as metabolic syndrome is a major, if not the major, risk factor for heart disease and diabetes. The Centers for Disease Control and Prevention now estimate that some 75 million Americans have metabolic syndrome. For those who have heart attacks, metabolic syndrome will very likely be the reason.

The first symptom doctors are told to look for in diagnosing metabolic syndrome is an expanding waistline. This means that if you’re overweight, there’s a good chance you have metabolic syndrome, and this is why you’re more likely to have a heart attack or become diabetic (or both) than someone who’s not. Although lean individuals, too, can have metabolic syndrome, and they are at greater risk of heart disease and diabetes than lean individuals without it.

Having metabolic syndrome is another way of saying that the cells in your body are actively ignoring the action of the hormone insulin — a condition known technically as being insulin-resistant. Because insulin resistance and metabolic syndrome still get remarkably little attention in the press (certainly compared with cholesterol), let me explain the basics.

You secrete insulin in response to the foods you eat — particularly the carbohydrates — to keep blood sugar in control after a meal. When your cells are resistant to insulin, your body (your pancreas, to be precise) responds to rising blood sugar by pumping out more and more insulin. Eventually the pancreas can no longer keep up with the demand or it gives in to what diabetologists call “pancreatic exhaustion.” Now your blood sugar will rise out of control, and you’ve got diabetes.

Not everyone with insulin resistance becomes diabetic; some continue to secrete enough insulin to overcome their cells’ resistance to the hormone. But having chronically elevated insulin levels has harmful effects of its own — heart disease, for one. A result is higher triglyceride levels and blood pressure, lower levels of HDL cholesterol (the “good cholesterol”), further worsening the insulin resistance — this is metabolic syndrome.

When physicians assess your risk of heart disease these days, they will take into consideration your LDL cholesterol (the bad kind), but also these symptoms of metabolic syndrome. The idea, according to Scott Grundy, a University of Texas Southwestern Medical Center nutritionist and the chairman of the panel that produced the last edition of the National Cholesterol Education Program guidelines, is that heart attacks 50 years ago might have been caused by high cholesterol — particularly high LDL cholesterol — but since then we’ve all gotten fatter and more diabetic, and now it’s metabolic syndrome that’s the more conspicuous problem.

This raises two obvious questions. The first is what sets off metabolic syndrome to begin with, which is another way of asking, What causes the initial insulin resistance? There are several hypotheses, but researchers who study the mechanisms of insulin resistance now think that a likely cause is the accumulation of fat in the liver. When studies have been done trying to answer this question in humans, says Varman Samuel, who studies insulin resistance at Yale School of Medicine, the correlation between liver fat and insulin resistance in patients, lean or obese, is “remarkably strong.” What it looks like, Samuel says, is that “when you deposit fat in the liver, that’s when you become insulin-resistant.”

That raises the other obvious question: What causes the liver to accumulate fat in humans? A common assumption is that simply getting fatter leads to a fatty liver, but this does not explain fatty liver in lean people. Some of it could be attributed to genetic predisposition. But harking back to Lustig, there’s also the very real possibility that it is caused by sugar.

As it happens, metabolic syndrome and insulin resistance are the reasons that many of the researchers today studying fructose became interested in the subject to begin with. If you want to cause insulin resistance in laboratory rats, says Gerald Reaven, the Stanford University diabetologist who did much of the pioneering work on the subject, feeding them diets that are mostly fructose is an easy way to do it. It’s a “very obvious, very dramatic” effect, Reaven says.

By the early 2000s, researchers studying fructose metabolism had established certain findings unambiguously and had well-established biochemical explanations for what was happening. Feed animals enough pure fructose or enough sugar, and their livers convert the fructose into fat — the saturated fatty acid, palmitate, to be precise, that supposedly gives us heart disease when we eat it, by raising LDL cholesterol. The fat accumulates in the liver, and insulin resistance and metabolic syndrome follow.

Michael Pagliassotti, a Colorado State University biochemist who did many of the relevant animal studies in the late 1990s, says these changes can happen in as little as a week if the animals are fed sugar or fructose in huge amounts — 60 or 70 percent of the calories in their diets. They can take several months if the animals are fed something closer to what humans (in America) actually consume — around 20 percent of the calories in their diet. Stop feeding them the sugar, in either case, and the fatty liver promptly goes away, and with it the insulin resistance.

Similar effects can be shown in humans, although the researchers doing this work typically did the studies with only fructose — as Luc Tappy did in Switzerland or Peter Havel and Kimber Stanhope did at the University of California, Davis — and pure fructose is not the same thing as sugar or high-fructose corn syrup. When Tappy fed his human subjects the equivalent of the fructose in 8 to 10 cans of Coke or Pepsi a day — a “pretty high dose,” he says —– their livers would start to become insulin-resistant, and their triglycerides would go up in just a few days. With lower doses, Tappy says, just as in the animal research, the same effects would appear, but it would take longer, a month or more.

Despite the steady accumulation of research, the evidence can still be criticized as falling far short of conclusive. The studies in rodents aren’t necessarily applicable to humans. And the kinds of studies that Tappy, Havel and Stanhope did — having real people drink beverages sweetened with fructose and comparing the effect with what happens when the same people or others drink beverages sweetened with glucose — aren’t applicable to real human experience, because we never naturally consume pure fructose. We always take it with glucose, in the nearly 50-50 combinations of sugar or high-fructose corn syrup. And then the amount of fructose or sucrose being fed in these studies, to the rodents or the human subjects, has typically been enormous.

This is why the research reviews on the subject invariably conclude that more research is necessary to establish at what dose sugar and high-fructose corn syrup start becoming what Lustig calls toxic. “There is clearly a need for intervention studies,” as Tappy recently phrased it in the technical jargon of the field, “in which the fructose intake of high-fructose consumers is reduced to better delineate the possible pathogenic role of fructose. At present, short-term-intervention studies, however, suggest that a high-fructose intake consisting of soft drinks, sweetened juices or bakery products can increase the risk of metabolic and cardiovascular diseases.”

In simpler language, how much of this stuff do we have to eat or drink, and for how long, before it does to us what it does to laboratory rats? And is that amount more than we’re already consuming?

Unfortunately, we’re unlikely to learn anything conclusive in the near future. As Lustig points out, sugar and high-fructose corn syrup are certainly not “acute toxins” of the kind the F.D.A. typically regulates and the effects of which can be studied over the course of days or months. The question is whether they’re “chronic toxins,” which means “not toxic after one meal, but after 1,000 meals.” This means that what Tappy calls “intervention studies” have to go on for significantly longer than 1,000 meals to be meaningful.

At the moment, the National Institutes of Health are supporting surprisingly few clinical trials related to sugar and high-fructose corn syrup in the U.S. All are small, and none will last more than a few months. Lustig and his colleagues at U.C.S.F. — including Jean-Marc Schwarz, whom Tappy describes as one of the three best fructose biochemists in the world — are doing one of these studies. It will look at what happens when obese teenagers consume no sugar other than what they might get in fruits and vegetables. Another study will do the same with pregnant women to see if their babies are born healthier and leaner.

Only one study in this country, by Havel and Stanhope at the University of California, Davis, is directly addressing the question of how much sugar is required to trigger the symptoms of insulin resistance and metabolic syndrome. Havel and Stanhope are having healthy people drink three sugar- or H.F.C.S.-sweetened beverages a day and then seeing what happens. The catch is that their study subjects go through this three-beverage-a-day routine for only two weeks. That doesn’t seem like a very long time — only 42 meals, not 1,000 — but Havel and Stanhope have been studying fructose since the mid-1990s, and they seem confident that two weeks is sufficient to see if these sugars cause at least some of the symptoms of metabolic syndrome.

So the answer to the question of whether sugar is as bad as Lustig claims is that it certainly could be. It very well may be true that sugar and high-fructose corn syrup, because of the unique way in which we metabolize fructose and at the levels we now consume it, cause fat to accumulate in our livers followed by insulin resistance and metabolic syndrome, and so trigger the process that leads to heart disease, diabetes and obesity. They could indeed be toxic, but they take years to do their damage. It doesn’t happen overnight. Until long-term studies are done, we won’t know for sure.

One more question still needs to be asked, and this is what my wife, who has had to live with my journalistic obsession on this subject, calls the Grinch-trying-to-steal-Christmas problem. What are the chances that sugar is actually worse than Lustig says it is?

One of the diseases that increases in incidence with obesity, diabetes and metabolic syndrome is cancer. This is why I said earlier that insulin resistance may be a fundamental underlying defect in many cancers, as it is in type 2 diabetes and heart disease. The connection between obesity, diabetes and cancer was first reported in 2004 in large population studies by researchers from the World Health Organization’s International Agency for Research on Cancer. It is not controversial. What it means is that you are more likely to get cancer if you’re obese or diabetic than if you’re not, and you’re more likely to get cancer if you have metabolic syndrome than if you don’t.

This goes along with two other observations that have led to the well-accepted idea that some large percentage of cancers are caused by our Western diets and lifestyles. This means they could actually be prevented if we could pinpoint exactly what the problem is and prevent or avoid that.

One observation is that death rates from cancer, like those from diabetes, increased significantly in the second half of the 19th century and the early decades of the 20th. As with diabetes, this observation was accompanied by a vigorous debate about whether those increases could be explained solely by the aging of the population and the use of new diagnostic techniques or whether it was really the incidence of cancer itself that was increasing. “By the 1930s,” as a 1997 report by the World Cancer Research Fund International and the American Institute for Cancer Research explained, “it was apparent that age-adjusted death rates from cancer were rising in the U.S.A.,” which meant that the likelihood of any particular 60-year-old, for instance, dying from cancer was increasing, even if there were indeed more 60-years-olds with each passing year.

The second observation was that malignant cancer, like diabetes, was a relatively rare disease in populations that didn’t eat Western diets, and in some of these populations it appeared to be virtually nonexistent. In the 1950s, malignant cancer among the Inuit, for instance, was still deemed sufficiently rare that physicians working in northern Canada would publish case reports in medical journals when they did diagnose a case.

In 1984, Canadian physicians published an analysis of 30 years of cancer incidence among Inuit in the western and central Arctic. While there had been a “striking increase in the incidence of cancers of modern societies” including lung and cervical cancer, they reported, there were still “conspicuous deficits” in breast-cancer rates. They could not find a single case in an Inuit patient before 1966; they could find only two cases between 1967 and 1980. Since then, as their diet became more like ours, breast cancer incidence has steadily increased among the Inuit, although it’s still significantly lower than it is in other North American ethnic groups. Diabetes rates in the Inuit have also gone from vanishingly low in the mid-20th century to high today.

Now most researchers will agree that the link between Western diet or lifestyle and cancer manifests itself through this association with obesity, diabetes and metabolic syndrome — i.e., insulin resistance. This was the conclusion, for instance, of a 2007 report published by the World Cancer Research Fund and the American Institute for Cancer Research — “Food, Nutrition, Physical Activity and the Prevention of Cancer.”

So how does it work? Cancer researchers now consider that the problem with insulin resistance is that it leads us to secrete more insulin, and insulin (as well as a related hormone known as insulin-like growth factor) actually promotes tumor growth.

As it was explained to me by Craig Thompson, who has done much of this research and is now president of Memorial Sloan-Kettering Cancer Center in New York, the cells of many human cancers come to depend on insulin to provide the fuel (blood sugar) and materials they need to grow and multiply. Insulin and insulin-like growth factor (and related growth factors) also provide the signal, in effect, to do it. The more insulin, the better they do. Some cancers develop mutations that serve the purpose of increasing the influence of insulin on the cell; others take advantage of the elevated insulin levels that are common to metabolic syndrome, obesity and type 2 diabetes. Some do both. Thompson believes that many pre-cancerous cells would never acquire the mutations that turn them into malignant tumors if they weren’t being driven by insulin to take up more and more blood sugar and metabolize it.

What these researchers call elevated insulin (or insulin-like growth factor) signaling appears to be a necessary step in many human cancers, particularly cancers like breast and colon cancer. Lewis Cantley, director of the Cancer Center at Beth Israel Deaconess Medical Center at Harvard Medical School, says that up to 80 percent of all human cancers are driven by either mutations or environmental factors that work to enhance or mimic the effect of insulin on the incipient tumor cells. Cantley is now the leader of one of five scientific “dream teams,” financed by a national coalition called Stand Up to Cancer, to study, in the case of Cantley’s team, precisely this link between a specific insulin-signaling gene (known technically as PI3K) and tumor development in breast and other cancers common to women.

Most of the researchers studying this insulin/cancer link seem concerned primarily with finding a drug that might work to suppress insulin signaling in incipient cancer cells and so, they hope, inhibit or prevent their growth entirely. Many of the experts writing about the insulin/cancer link from a public health perspective — as in the 2007 report from the World Cancer Research Fund and the American Institute for Cancer Research — work from the assumption that chronically elevated insulin levels and insulin resistance are both caused by being fat or by getting fatter. They recommend, as the 2007 report did, that we should all work to be lean and more physically active, and that in turn will help us prevent cancer.

But some researchers will make the case, as Cantley and Thompson do, that if something other than just being fatter is causing insulin resistance to begin with, that’s quite likely the dietary cause of many cancers. If it’s sugar that causes insulin resistance, they say, then the conclusion is hard to avoid that sugar causes cancer — some cancers, at least — radical as this may seem and despite the fact that this suggestion has rarely if ever been voiced before publicly. For just this reason, neither of these men will eat sugar or high-fructose corn syrup, if they can avoid it.

“I have eliminated refined sugar from my diet and eat as little as I possibly can,” Thompson told me, “because I believe ultimately it’s something I can do to decrease my risk of cancer.” Cantley put it this way: “Sugar scares me.”

Sugar scares me too, obviously. I’d like to eat it in moderation. I’d certainly like my two sons to be able to eat it in moderation, to not overconsume it, but I don’t actually know what that means, and I’ve been reporting on this subject and studying it for more than a decade. If sugar just makes us fatter, that’s one thing. We start gaining weight, we eat less of it. But we are also talking about things we can’t see — fatty liver, insulin resistance and all that follows. Officially I’m not supposed to worry because the evidence isn’t conclusive, but I do.

Gary Taubes (gataubes@gmail.com) is a Robert Wood Johnson Foundation independent investigator in health policy and the author of “Why We Get Fat.”

Source: Organic Consumers Association/New York Times

The Five Signs of Stroke

Franciscan Health System supports stroke education during National Stroke Awareness Month.
The St. Joseph Medical Center (SJMC) Stroke Care program was recognized as a Center of Excellence and earned the Gold Seal of Approval™ from the Joint Commission for primary stroke centers.
Learn from SJMC Stroke Coordinator Gena Kreiner, RN, as she discusses the five signs of stroke and ways to reduce the associated risk factors.

Source:
Franciscanhealth on YouTube

Certificate of Confidentiality

Certificates of Confidentiality

• Certificate of Confidentiality Application Instructions
• Frequently Asked Questions

Purpose

Certificates of Confidentiality are issued by the Centers for Disease Control and Prevention (CDC) to protect the privacy of research subjects by protecting investigators and institutions from being compelled to release information that could be used to identify subjects with a research project. Certificates of Confidentiality are issued to institutions or universities where the research is conducted. They allow the investigator and others who have access to research records to refuse to disclose identifying information in any civil, criminal, administrative, legislative, or other proceeding, whether at the federal, state, or local level.

Identifying information is broadly defined as any item or combination of items in the research data that could lead directly or indirectly to the identification of a research subject.

By protecting researchers and institutions from being compelled to disclose information that would identify research participants, Certificates of Confidentiality help achieve the research objectives and promote participation in studies by assuring privacy to subjects.

Statutory Authority

Under section 301(d) of the Public Health Service Act (42 U.S.C. 241(d)) the Secretary of Health and Human Services may authorize persons engaged in biomedical, behavioral, clinical, or other research to protect the privacy of individuals who are the subjects of that research. This authority has been delegated to the Centers for Disease Control and Prevention (CDC).

Persons authorized by the CDC to protect the privacy of research subjects may not be compelled in any federal, state, or local civil, criminal, administrative, legislative, or other proceedings to identify them by name or other identifying characteristic.

Extent and Limitations of Coverage

Certificates can be used for biomedical, behavioral, clinical or other types of research that is sensitive. Research data is sensitive when disclosure of identifying information could have adverse consequences for subjects or damage their financial standing, employability, insurability, or reputation.

Examples of sensitive research activities include but are not limited to the following:

• Collecting genetic information;
• Collecting information on psychological well-being of subjects;
• Collecting information on subjects’ sexual attitudes, preferences or practices;
• Collecting data on substance abuse or other illegal risk behaviors;
• Studies where subjects may be involved in litigation related to exposures under study (e.g., environmental or occupational exposures).

In general, certificates are issued for single, well-defined research projects rather than groups or classes of projects.

A Certificate of Confidentiality protects personally identifiable information about subjects in the research project while the Certificate is in effect. Generally, Certificates are effective on the date of issuance or upon commencement of the research project if that occurs after the date of issuance. The expiration date should correspond to the completion of the study. The Certificate will state the date upon which it becomes effective and the date upon which it expires. A Certificate of Confidentiality protects all information identifiable to any individual who participates as a research subject (i.e., about whom the investigator maintains identifying information) during any time the Certificate is in effect. An extension of coverage must be requested if the research extends beyond the expiration date of the original Certificate. However, the protection afforded by the Certificate is permanent. All personally identifiable information maintained about participants in the project while the Certificate is in effect is protected in perpetuity. Some projects are ineligible for a Certificate of Confidentiality. To be eligible for a CDC Certificate, a project must be: (1) research, (2) funded by CDC, (3) collecting personally identifiable information that is sensitive and, if disclosed, could significantly harm or damage the participant, and (4) reviewed and approved by IRB(s).

While Certificates protect against involuntary disclosure, investigators should note that research subjects might voluntarily disclose their research data or information. Subjects may disclose information to physicians or other third parties. They may also authorize in writing the investigator to release the information to insurers, employers, or other third parties. In such cases, researchers may not use the Certificate to refuse disclosure. Moreover, researchers are not prevented from the voluntary disclosure of matters such as child abuse, reportable communicable diseases, or subject’s threatened violence to self or others. (For information on communicable disease reporting policy, see Notifiable Disease Reporting with Confidentiality Certificates). However, if the researcher intends to make any voluntary disclosures, the consent form must specify such disclosure.

Certificates do not authorize researchers to refuse to disclose information about subjects if authorized DHHS personnel request such information for an audit or program evaluation. Neither can researchers refuse to disclose such information if it is required to be disclosed by the Federal Food, Drug, and Cosmetic Act.

In the informed consent form, investigators should tell research subjects that a Certificate is in effect. Subjects should be given a fair and clear explanation of the protection that it affords, including the limitations and exceptions noted above. Every research project that includes human research subjects should explain how identifiable information will be used or disclosed, regardless of whether or not a Certificate is in effect. The Office of Human Subjects Protection (OHRP) provides guidance on the content of informed consent documents.

Assurance of Confidentiality

Purpose

An Assurance of Confidentiality is a formal confidentiality protection authorized under Section 308(d) of the Public Health Service Act. It is used for projects conducted by CDC staff or contractors that involve the collection or maintenance of sensitive identifiable or potentially identifiable information. This protection allows CDC programs to assure individuals and institutions involved in research or non-research projects that those conducting the project will protect the confidentiality of the data collected. The legislation states that no identifiable information may be used for any purpose other than the purpose for which it was supplied unless such institution or individual has consented to that disclosure.

Statutory Authority

Under section 308(d) of the Public Health Service Act surveys conducted by the National Center for Health Statistics (NCHS) as part of their authorizing legislation are automatically protected by an Assurance of Confidentiality. In addition, Assurances of Confidentiality may be issued to projects conducted by all other CDC components, after formal application to and approval by the CDC Confidentiality Review Group has been obtained.

Information about institutions and/or individuals of research or non-research projects that involve the collection or maintenance of sensitive identifiable or potentially identifiable information and for which an Assurance of Confidentiality has been approved is protected. At CDC, the 308(d) assurance has most often been used to protect sensitive identifiable data for non-research projects, but has also been used for research studies collecting sensitive identifiable data.

Extent and Limitations of Coverage

Protected information includes identifiable or potentially identifiable information on institutions or individuals who are the subjects of research or non-research studies with an approved Assurance of Confidentiality.

Disclosures can be made without individual authorization only for purposes stated at the time of data collection or specifically consented to thereafter by each of the parties who were provided the promise of confidentiality.

Certificates and Assurances of Confidentiality do not take the place of good data security or clear policies and procedures for data protection, which are essential to the protection of participants’ privacy. Investigators should take appropriate steps to safeguard data and findings. Unauthorized individuals must not access the data or learn the identity of participants.

Certificates and Assurances of Confidentiality Contact
Phone: 404-639-4642
Email: cdccoc@cdc.gov

Source: CDC

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Signs of Infertility in Men and Women

by Anna Short 

Infertility is a problem that many couples face. Most do not realize that they have a fertility problem until they try and fail to conceive over a period of 12 months or more. Because the cause of infertility may be either with the man or the woman, it’s important to look at signs of infertility for both members of a couple trying to get pregnant. Being aware of some of these signs can help you get a diagnosis before you spend months trying to get pregnant with no luck.

Signs of Infertility in Women

1. Irregular menstrual cycles. If you have a period only occasionally, or if your cycles are less than 24 days long or more than 35 days long, it’s worth talking to your doctor about whether you might have problems ovulating.

2. Unusual bleeding or cramps. Normal periods can include anywhere from 3 to 7 days of bleeding. If your periods fall outside these time frames, or if they are either unusually light and spotty or unusually heavy and intense and accompanied by cramping, it may be a sign of infertility. If you are experiencing these symptoms, your doctor might also ask about any changes in the coloring of the blood, as this information can be helpful for a diagnosis.

3. Excess weight. If your BMI is very high, you may be at risk for hormonal imbalances that can affect your ability to get pregnant.

4. Too Little Weight. Weight concerns can arise on the other end of the spectrum too. Women who are much too thin may not be consuming all the nutrients necessary for a healthy reproductive system.

5. Advanced Maternal Age. If you are over 35, you should consider having your doctor go ahead and check your hormonal levels even if you haven’t been trying to conceive for very long.

6. Successive Miscarriages. While miscarriages are not that uncommon, several successive miscarriages could indicate a problem with a woman’s ability to carry to term in the future. There are often measures that can be taken to decrease the likelihood of future miscarriages.

7. Use of insulin or thyroid hormones. These medications can lead to irregular menstrual cycles. Some antidepressants are also possible risk factors, so disclose all medications you are taking to your doctor.

Signs of Infertility in Men

1. Erectile Dysfunction or Ejaculatory Problems. While not necessarily a definitive sign of low sperm count or poor sperm mobility, it can be a factor worth looking into.

2. Anatomic abnormalities. Undescended testicles can be a factor of infertility.

3. Excessive Weight. As with women, obesity in a man can affect the hormones necessary for producing the right amount of sperm. Obesity in a man may also affect the body in such a way that the sperm it does produce are not properly formed. Malformed sperm are often unable to penetrate the woman’s eggs, a critical part of conception.

4. Use of Tagamet or hypertension medication. These medications can cause male factor infertility (low sperm count, low motility or malformed sperm).

For Both of You

1. Chronic illness. Diabetes and hyperthyroidism in particular are known to interfere with fertility in men and women. See the gender-specific discussions above regarding medicines used to treat these conditions.

2. Past Cancer Treatments. In particular, if either of you had radiation therapy near reproductive organs, a follow up with your doctor is a good idea.

3. Sexually Transmitted Diseases. In women, chlamydia or gonorrhea may led to blockages of the fallopian tubes that will need to be reversed if possible. Because symptoms of these STDs are often not evident in women, have frank discussions with your partner about each of your sexual histories and get screened if there might be a concern.

4. Drinking, smoking and yes, marijuana use. All of these increase the chances that either one of you will experience fertility problems. It’s best to quit these habits long before you begin trying to conceive.

About the Author

Anna Short has developed expertise on infertility through a combination of personal experience and thorough research. For more great information on signs of infertility, visit http://www.infertility-options-info.com. Be sure to check out her free email course on infertility.

Source: GoArticles.com

Prostate Cancer – Today Show Al Roker

Uploaded by RoboticOncology on Sep 28, 2010

September is Prostate Cancer Awareness Month. Prostate cancer is a disease that affects 1 out of every 6 men. Early prostate cancer detection and treatment can mean the difference between life and death. The good news from Dr. David Samadi, Chief of Robotics and Minimally Invasive at Surgery at the Mount Sinai Medical Center, is that he’s able to provide invaluable recommendations and guidance about prostate cancer screening and treatment. The average age of men with prostate cancer is 69, but there are several other factors (including genetic history and ethnicity) that can contribute to the likelihood of men developing this disease.To learn more about prostate cancer diagnosis and treatment, visit www.roboticonconcology.com or www.smart-surgery.com.

 Source: RoboticOncology on YouTube

Talking to Your Family About Kidney Disease

 

 

Talking to Your Family About Kidney Disease

• Why should my family know about kidney disease?
• What should I tell my family about kidney disease?
• How can I help my family prevent kidney failure?
• T.E.S.T. your family members
• Where can I get more information?

Why should my family know about kidney disease?

• Kidney disease runs in families.
• Even if only one person in a family has kidney failure, all blood relatives should be tested for kidney disease.
• With early treatment, kidney disease can be slowed and dialysis or a transplant may be avoided.

What should I tell my family about kidney disease?

• Diabetes and high blood pressure are the leading causes of kidney failure.
• Managing your blood sugar and blood pressure may help the kidneys stay healthy.
• Get tested for kidney disease because it runs in families.
• Blood and urine tests are the only way to find out if you have kidney disease because there are no early warning signs.
• Finding kidney disease early and treating it can slow kidney damage and may prevent kidney failure.

How can I help my family prevent kidney failure?

Tell your family members to talk to their doctors about getting tested for kidney disease. Doing this may be difficult, but it can help save their lives.

T.E.S.T. your family members

• Teach them that kidney disease runs in families.
• Encourage them to get tested for kidney disease.
• Support their efforts to manage their diabetes and high blood pressure.
• Tell them where they can find more information.

Where can I get more information?

NKDEP provides free educational materials and resources for patients and their families.

Last Reviewed: June 30, 2010

Source:

NKDEP is an initiative of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK),
National Institutes of Health (NIH), U.S. Department of Health & Human Services (DHHS).

U.S. Department of
Health & Human Services

National Institutes
of Health

Diagnosing Autism

Diagnosing Autism

Source: LocalNews – GrabNetworks

While a newborn probably won’t show autism symptoms, the developmental disorder may manifest as early as 18 months. At this infant age, diagnosing autism starts with a behavioral analysis and a test, like the checklist for autism in toddlers.

The Audacity of Genetically Modified Foods

The Audacity of Genetically Modified Foods

by Bruce Robinson

The biotech industry, led by Monsanto, promotes the idea that the arguments about genetically modified crops should focus on the science and the economics as Monsanto sees them. I maintain that the real discussion should be about the audacity and illegitimate way GM crops have been forced on a reluctant United States and world — the money, corruption, politics and obfuscation that characterize its rise to dominance. The discussion should focus on how GM crops have taken over our food supply with little concern for safety or our right to choose.

Does it bother you that we consumers are largely unaware that 70 percent to 80 percent of the processed foods we buy contain GM ingredients? We are “largely unaware” because these foods are not labeled — even though 90 percent of Americans want them labeled and think that we have the right to know what is in our food. The biotech industry fights labeling viciously because they know that, if GM foods were labeled, many would refuse to buy them as is the case in Europe. It`s not financial considerations that leave us with no choice; it`s our lack of awareness that allows them to take advantage of us. How many realize that Kraft Mac & Cheese is non-GM in Europe but does contain GM ingredients in the United States?

Our regulatory bodies and government are staffed with pro-GM people, a veritable revolving door. Michael Taylor, a Monsanto lawyer, moved from Monsanto to the Food and Drug Administration where he wrote the rules that were used to justify the release of Monsanto`s bovine growth hormone RBGH. He then returned to Monsanto as vice president. He currently is the FDA deputy commissioner for foods — not the best place for a person with such apparent bias. And Supreme Court Justice Clarence Thomas, previously general counsel for Monsanto, supported a ruling that GM alfalfa could be released. He does not recuse himself in cases like this involving conflict of interest.

There are minimal requirements for independent testing of GM crops and foods. Testing is left to the biotech companies who then choose which tests to submit to our regulatory bodies. This results from the gift of “substantial equivalence” that says we don`t need to do thorough testing because GM crops are substantially equivalent to regular crops. But how can we know they are substantially equivalent if we don`t thoroughly test them? Who do our regulatory bodies represent? Aren’t they in place to protect our health? Shouldn’t they be doing or overseeing the testing in our interest?

There is significant correlation between the increase in incidence of serious health problems and the introduction of various GM crops into our foods. Check out Robyn O`Brien`s “The Unhealthy Truth.” Why would the incidence of peanut allergies begin increasing 20 percent yearly just after GM soy came into widespread use in the United States in 1996? Why would the incidence of soy allergies increase by 50 percent in 1998, the year GM soy was introduced in the United Kingdom? Correlation is not the same as cause and effect but determining cause is almost impossible when foods are not labeled.

What can we learn from the numerous cases where wild or domestic animals refuse to eat GM crops but willingly eat the non-GM equivalent? Even more drastic are the cases of animals dying following their consumption of GM crops — not only lab test animals but farm animals. Obviously changes are occurring within the plant that go way beyond what was intended. I remember a statement from Chris Bright that “nature is a system of unfathomable complexity.” Any messing with it should proceed with much greater caution than we are seeing today.

Roundup Ready GM alfalfa has been approved by the Department of Agriculture and is about to be grown large scale and will become the food for much of our meat and dairy animals. Alfalfa is water-intensive and has no significant weed problem while being extremely effective at contaminating other crops. I think this counter-intuitive agriculture policy is indicative of the revolving door and its attendant corruption.

Dominance of GM crops and food results in suppressing the growth of organic agriculture as well as traditional, non-GM, agriculture. Contamination, super weeds and constant efforts to weaken organic standards truly threaten the vibrant organic food industry in Colorado and the nation.

Monsanto and the biotech industry are well on their way to controlling the world`s seed markets. This, together with the lack of labeling, denies us freedom of choice in what we buy. It also dominates and controls farmers worldwide — what they plant and how they operate.

Our favorite fruits, vegetables and grains are being readied for the GM market that views us as guinea pigs. Why are we and our elected representatives allowing them to do this to us? I highly recommend “Seeds of Deception” by Jeffrey Smith as well as his Web site: responsibletechnology.org. Resistance to GM foods is increasing rapidly and this Web site offers strategies and tools for involvement in this critical issue.

About The Author:

Bruce Robinson, a retired software developer, lives in Boulder, Colorado

Source

Published on Sunday, May 8, 2011 by the © Boulder Daily Camera

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