Marc Joseph Nutrition - Blog

Oh my:

[T]he intersection of money and medicine, and its effect on the well-being of patients, has become one of the most contentious issues in health care. Nowhere is that more true than in psychiatry, where increasing payments to doctors have coincided with the growing use in children of a relatively new class of drugs known as atypical antipsychotics.

These best-selling drugs, including Risperdal, Seroquel, Zyprexa, Abilify and Geodon, are now being prescribed to more than half a million children in the United States to help parents deal with behavior problems despite profound risks and almost no approved uses for minors.

A New York Times analysis of records in Minnesota, the only state that requires public reports of all drug company marketing payments to doctors, provides rare documentation of how financial relationships between doctors and drug makers correspond to the growing use of atypicals in children.

From 2000 to 2005, drug maker payments to Minnesota psychiatrists rose more than sixfold, to $1.6 million. During those same years, prescriptions of antipsychotics for children in Minnesota’s Medicaid program rose more than ninefold.

Those who took the most money from makers of atypicals tended to prescribe the drugs to children the most often, the data suggest. On average, Minnesota psychiatrists who received at least $5,000 from atypical makers from 2000 to 2005 appear to have written three times as many atypical prescriptions for children as psychiatrists who received less or no money.

The excerpt above is from a recent NY Times article that provides an excellent “behind-the-scenes” look at the use and marketing of prescription antipsychotic drugs for children. It’s truly eye-opening. Read the whole thing.

Unfortunately, Minnesota is the only state that requires disclosure of drug company marketing payments to doctors. It would be great to see the entire industry-wide picture — and not just for psychiatric drugs.

Increasing Number of Diagnoses

Another question worth answering is why has there been such an increase in the perceived need for using these drugs with children?

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In a recent study published in the American Journal of Clinical Nutrition, researchers have found that the current Adequate Intake (AI)* for choline may not be sufficient to prevent fatty liver and muscle damage.

*An AI is a suggested intake in place of a Recommended Daily Allowance (RDA) in cases where there is insufficient scientific information to make a definitive intake recommendation.

Specifically, the scientists gave the study participants 550 mg choline per day (the AI for men) for every 70 kg in body weight for 10 days, followed by a diet of < 50 mg choline (plus 400 mcg of folic acid in some participants).

When given the choline deprived diet, 77% of the men and 80% of the post-menopausal women developed fatty liver or muscle damage, whereas only 44% of pre-menopausal women developed such signs. Estrogen increases the body’s production of phosphatidylcholine (see below) and may account for this observed difference.

Notably, nearly 1/4 of the men in the study developed signs of fatty liver and muscle damage while consuming the current AI level of choline.

Choline - What is It and Why Should You Care?

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In a recent study published in the journal Cell, Canadian scientists identified a breakthrough understanding of the role of pain nerves in insulin-producing (islet) cells, and in turn, learned how to prevent pancreatic cell inflammation and reverse Type 1 diabetes in mice.

The researchers found that the nerve receptors in the islet cells of non-obese diabetic (NOD) mice were not secreting enough neuropeptides, chemical compounds that can help nerve cells to communicate with one another and regulate physiologic processes.

When scientists supplied these diabetic-prone mice with neuropeptide substance P, which acts as both a neurotransmitter and neuromodulator and plays a key role in pain transmission, islet cell inflammation subsided in one day and insulin sensitivity returned to normal for a period of weeks.

Apparently, there is a key “control circuit” between the insulin-producing cells in the pancreas and the associated pain nerves:

“We started to look at nervous system elements that seemed to play a role in Type 1 diabetes and found that specific sensory neurons are critical for islet immune attack in the pancreas,” said Dr. Hans Michael Dosch, the principal investigator. “These nerves secrete insufficient neuropeptides which sustain normal islet function, creating a vicious circle of progressive islet stress.” …

… “The major discovery was that removal of sensory neurons expressing the receptor TRPV1 neurons in NOD mice prevented islet cell inflammation and diabetes in most animals, which led us to fundamentally new insights into the mechanisms of this disease,” said Dr. Michael Salter, co-principal investigator, senior scientist at SickKids, professor of Physiology and director of the Centre for the Study of Pain at the University of Toronto. “Disease protection occurred despite the fact that autoimmunity continues in the animals. This helped us to focus our studies on finding the new control circuit in the islets.”

Potential Future Application in Type 2 Diabetes

This discovery is big news. Researchers are currently looking to test the approach in human trials and also to extend the study to the much more prevalent Type 2 (obesity-associated) diabetes and potentially other autoimmune conditions.

In Type 1 diabetes, islet cells in the pancreas do not produce insulin, and affected individuals must get daily insulin injections to manage blood glucose levels.

In Type 2 diabetes, the body’s cells become insensitive to the action of insulin, and the body may also eventually stop producing sufficient insulin.

You can learn more about Type I and Type II diabetes, their potential causes, and my treatment approaches that focus on addressing nutritional and environmental factors here.

(Image Credit: HowStuffWorks)

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Discover How Nutrition Can Make a Difference in Your Life …

Marc Joseph Nutrition

A recent New York Times article highlighted what has become a growing trend over the last few years: giving multiple psychiatric medications to children:

[A] growing number of children and teenagers in the United States are taking not just a single drug for discrete psychiatric difficulties but combinations of powerful and even life-threatening medications to treat a dizzying array of problems.

Last year in the United States, about 1.6 million children and teenagers — 280,000 of them under age 10 — were given at least two psychiatric drugs in combination, according to an analysis performed by Medco Health Solutions at the request of The New York Times. More than 500,000 were prescribed at least three psychiatric drugs. More than 160,000 got at least four medications together, the analysis found.

The numbers are amazing, aren’t they?

The article notes that there is evidence that suggests individual medications may be useful for certain conditions, but that there is “virtually no scientific evidence to justify this multiplication of pills.”

The majority of the child prescriptions are for ADD/ADHD and depression (click image to expand):

What’s going on here? Stimulants, antidepressants, antipsychotics and anticonvulsants in young children? Why the greater use of these serious drugs (many with significant risk for side effects)? Most importantly, why the increasing prevalence of conditions in children requiring their use?

I think dietary factors and toxin exposure likely play significant roles in the greater prevalence of these conditions and the use of these drugs in children. Taking multiple prescription drugs without a closer look at potential root causes doesn’t seem to make much sense.

The behavior of many children (and adults) with attention deficit disorders often significantly improves with a shift to a whole foods diet that eliminates chemical additives. For others, exposure to toxins, such as those found in some vaccines and in the environment at large, may be an underlying cause. Safely reducing a child’s toxic body burden may help to improve the situation.

You can read more about a better approach to ADD/ADHD that attempts to identify and address underlying root causes here.

In a study recently published in the Journal of the American Medical Association, researchers found that Caucasians with the highest vitamin D levels (25-hydroxyvitamin D > 99.1 nmol/L) had a 62% lower risk of developing multiple sclerosis (MS) than those people with the lowest vitamin D levels (< 66.3 nmol/L). The inverse relationship between MS and vitamin D level was especially strong for people younger than 20 years.

This study adds to a fairly substantial body of earlier research that suggests vitamin D may play an important role in MS. Here’s a good overview article on the topic, as well as a map showing how MS cases seem to vary by latitude.

I’ve posted several times in the past about the importance of vitamin D in helping to prevent the development of various conditions:

• Epidemic Influenza and Vitamin D
• Vitamin D Deficiency Increases Risk of Nursing Home Admission
• Vitamin D Could Reduce Pancreatic Cancer Risk
• Vitamin D Deficiency During Pregnancy

Making sure that your vitamin D levels (25-hydroxyvitamin D) are at least in the high end of the normal range (45-50 ng/mL or 112-125 nmol/L) year-round is a smart step for ensuring better health.

Researchers at San Diego’s Scripps Research Institute recently published a study that found mice that were genetically altered to have a reduced core body temperature had a significantly greater average lifespan (12% in males, 20% in females) than non-altered mice.

In the past, other studies have noted that:

• Body temperature and aging are related in cold-blooded animals.
• Calorie-restriction (CR) can increase lifespan in warm-blooded animals and also results in a lowered body temperature.

However, this was the first study to find that a sustained decrease in core body temperature could increase lifespan in warm-blooded animals independently of calorie-restriction or an altered diet.

Prior to the current study, critical questions about the relation between calorie restriction, core body temperature, and lifespan remained unanswered. Was calorie restriction itself responsible for longer lifespan, with reduced body temperature simply a consequence? Or was the reduction of core body temperature a key contributor to the beneficial effects of calorie restriction?

To find out, the researchers genetically altered the mice to over-express a protein in the hypothalamus, the part of the brain responsible for regulating body temperature. This protein change increased the hypothalamus temperature, which, in turn, resulted in a decrease in body temperature of approximately 0.5 to 1.0 degree farenheit.

The altered mice had normal ability to generate fever and were just as active as the other mice. Most importantly, the altered mice were allowed to eat as much food as they wanted, and ate about the same as the control mice. They also weighed about 10 percent more than the control mice (less energy required to maintain the lower body temperature).

The exact mechanisms as to how the decrease in body temperature may lengthen life remain to be discovered (Hormonal effects? Reduced oxidative stress?), but this finding is certainly an interesting and important one. The results reinforce just how important those small structures at the base of your brain, like the hypothalamus, are to your overall health. Small changes in function can make big differences.

An announcement that didn’t make the major newspaper headlines, but is nevertheless big news. Researchers at the Linus Pauling Institute at Oregon State University (OSU) have discovered a new technique that allows them to observe and accurately measure the level of a key oxidant (superoxide) in animal cells.

Prior to this, there was no direct and accurate way to measure superoxide or its origin from the two places that produce it, the cell’s cytosol or mitochondria. Now there is.

With the new system developed at OSU, researchers can use a fluorescent microscope, a fairly standard laboratory tool, to actually see levels of superoxide and observe changes as experiments are performed with living cells.

Oxidation is a process that occurs naturally in the body — for example, in cell energy production and some immune reactions. As a result of the process, unstable atoms and molecules (e.g., free radicals such as superoxide) can be formed.

The body produces substances (e.g., glutathione, superoxide dismutase, catalase) that help to stabilize these atoms and molecules and prevent excessive damage and inflammation. We also take in anti-oxidants through our diet, in the form of different nutrients such as vitamins C and E, that help to neutralize these free radicals.

When these free radicals accumulate, cell structures can be damaged. This damage is believed to play an important role in many degenerative diseases, including ALS, Parkinson’s, Alzheimer’s, heart disease, hypertension, diabetes, and more.

The discovery of this technique will help researchers better understand what’s really happening in cells, as well as the effects of different potential treatments, and should help to speed research in many diseases. It’s definitely good news.

In this American Journal of Clinical Nutrition editorial, the authors discuss the important issue of vitamin D deficiency during pregnancy.

The authors mention a recent study of women in the Netherlands, and note that the study found that >50% (!) of darker-skinned women were deficient in vitamin D (whereas only 8% of fairer-skinned women were).

But the numbers were likely even worse than those. The study used a very conservative level of vitamin D to indicate vitamin D deficiency, one that was likely much too low.

The correct vitamin D form to measure for deficiency is 25-hydroxyvitamin D. The study used 25 nmol/L as the cut-off, while levels closer to 80 nmol/L are increasingly being shown in research to be optimal.

As the editorial notes, Vitamin D levels during pregnancy and the early years of development are critical not only for bone development, but also for the immune system and nervous system development — and may have lifelong implications.

It is difficult to get adequate vitamin D through the diet, since dairy is really the only food category that contains significant amounts of the nutrient.

The primary source of vitamin D is from sunshine. The sun’s UV-B rays hit the skin and a molecule is converted that starts a multi-step process toward the formation of active vitamin D in the body. Exposure to mid-day summer sun at the beach can generate up to 20,000 IU of active vitamin D.

In Northern latitudes during the winter months, the sun’s rays are not strong enough to generate sufficient vitamin D levels. Also, individuals with darker skin require significantly greater levels of sun exposure to generate adequate amounts of vitamin D.

Unfortunately, the U.S. government’s current recommended adequate intake level for vitamin D (200 to 600 IU) is set way below the level necessary to maintain vitamin D near optimal levels. As discussed here, adequate daily intake levels may be at least 2,000 IU/day, and possibly higher, for individuals not getting regular, limited sun exposure*.

During the winter months and in groups of people with limited sun exposure (e.g., infants, the elderly, darker-skinned people spending lots of time indoors), supplementation with vitamin D, either in the form of cholecalciferol or obtained via a good quality (toxin-free) cod liver oil will likely be important in helping to maintain adequate vitamin D levels.

(Vitamin D is a critically important nutrient that is commonly deficient. I’ll regularly revisit this topic in future posts.)

* Note: Neither vitamin D researchers or I are suggesting that you should spend a lot of time in the sun. Excessive exposure to the sun’s rays can damage the skin. The amount of exposure required for adequate vitamin D formation is brief — 10 to 15 minutes a day on the exposed arms/neck/face a few times a week during spring, summer, and early fall.