Marc Joseph Nutrition - Blog

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.

A recent study in the Journal of the American Medical Association examined different midlife risk factors and their association with survival rates in men.

Researchers found that 42% of the study’s 5820 original study participants survived to the age of 85. However, only 11% of the study participants survived to 85 years without getting one of 6 major chronic diseases and without physical and cognitive impairment (a state referred to by the authors as “exceptional survival”).

Participants who had high (hand) grip strength and avoided risk factors, including:

• Becoming overweight
• High blood pressure
• High blood sugar
• Smoking
• Excessive alcohol consumption

in mid-life had a greater chance of both reaching age 85 and exceptional survival.

Being married and avoiding high triglycerides were also associated with exceptional survival. Being single, on the other hand, was not associated with reaching age 85.

Researchers estimated that the probability of survival to 85 may be as high as 69% for men with no risk factors and as low as 22% with six or more risk factors. Exceptional survival to age 85 was estimated as high as 55% for men with no risk factors and as low as 9% with six or more risk factors.

Those are some pretty big differences. Nutrition plays a significant role in many of the risk factors - e.g., high blood sugar, high blood pressure, and more. There’s clearly a lot that an individual can do well before reaching older age to both lengthen and improve the quality of life.

The Union of Concerned Scientists has just released The A to Z Guide to Political Interference in Science:

In recent years, scientists who work for and advise the federal government have seen their work manipulated, suppressed, distorted, while agencies have systematically limited public and policy maker access to critical scientific information. To document this abuse, the Union of Concerned Scientists has created the A to Z Guide to Political Interference in Science.

The guide highlights environmental, public health, pollution, and national security issues using a periodic table design:

Lots of interesting issues are profiled, including federal government and industry interference in science involving mercury, lead, pesticides, and Ground Zero air pollution.

Check it out …

Bad news if you live near or downwind of an existing cement manufacturing plant.

(That would be many folks in the Northeast, north-Midwest, north Texas, north and east of Los Angeles, and elsewhere. Here’s an interactive map showing the locations of cement kilns in the U.S.)

The EPA denied two court orders to set restrictions on mercury emissions from cement kilns, and instead ruled that only plants built after December 2005 will have to limit and measure emissions.

Older cement kilns get EPA pass on mercury

EPA Fails to Limit Toxic Mercury Pollution from Cement Kilns

Mercury is a known potent neurotoxin. The EPA estimates 1 in 6 women of childbearing age have unsafe blood mercury levels. Also, autism rates have been found to be significantly higher in areas with higher mercury emissions.

Industry lobbying seems to have paid off:

Parts of the decision, signed late Friday by EPA Administrator Stephen L. Johnson, closely follow industry requests to the agency. Industry officials also met with White House staffers Nov. 30 to discuss the pending decision, and EPA staffers phoned in to the meeting, records show.

1997 EPA data suggests that that cement kilns account for less than five percent of all mercury emissions (created when mercury is released from limestone when heated during the manufacture of cement). However, it seems as though cement manufacturers may have been drastically understating their emission estimates:

Although federal law requires cement plants to report their mercury emissions, it does not require those reports to be based on actual measurements. Where kilns have tested their emissions, the data has shown their earlier “reporting” to be gross understatements of actual emissions. For example, a plant located in Alpena, Michigan, routinely reported emissions of approximately 50 pounds of mercury per year. But when the Michigan Department of Environmental Quality required the cement plant to test their actual stack emissions, it turned out the kiln was really emitting 581 pounds of mercury. A similar instance of underreporting has been uncovered at a cement plant in Oregon, which is the nation’s third worst mercury polluter.

“If reporting from the rest of the cement industry is as inaccurate as the reporting from Alpena, this industry could be putting out between 25 and 50 tons of mercury every year,” said Jane Williams, Chair of Sierra Club’s Air Toxics Task Force. “That would put cement kilns in the same category as coal-fired power plants, which have long been recognized as the worst culprit for mercury contamination.”

Cement manufacturers argue that it would be too costly and ineffective to implement measures to restrict mercury emissions, but environmental groups disagree:

EPA environmental engineer Keith Barnett, of the agency’s air-quality planning and standards office in North Carolina, said it would cost a cement manufacturer “$1.5 million per year per kiln for a wet scrubber” that might reduce emissions by 42%, which he said was not a large enough reduction to justify the cost.

Marti Sinclair of the Sierra Club said $1.5 million would be a small price to protect the public, noting that one of the nation’s leading cement producers had reported revenue of $1.1 billion last year and had already installed such technology in Switzerland, where it was required.

I have to side with the latter group. $1.5M per kiln seems like a small price to pay for reducing mercury emissions by nearly half.

More background on the issue is available here.

If the EPA’s decision strikes you as a poor one, write your Congresspersons and ask for them to push for a review of the decision.

Autistic individuals often have an impaired ability to interpret social cues as communicated through speech intonation, eye movements, and body language. Researchers have theorized that autistic individuals may have lower levels of a hormone called oxytocin, and that the deficiency may help to explain some of the impaired ability to interpret social cues.

Oxytocin is a hormone secreted by the pituitary gland, which is located at the base of the brain. In women, the hormone stimulates contractions of the uterus during labor and release of milk during breast-feeding. In both men and women, oxytocin is associated with increased feelings of trust, commitment, empathy, and compassion.

In a study from earlier this summer:

Oxytocin Increases Retention of Social Cognition in Autism.

researchers found that autistic adults given oxytocin showed improved ability to interpret emotion in speech comprehension tasks.

And, now, in a more recent study of non-autistic individuals, researchers have found that oxytocin seems to also improve the ability to interpret the mental state of others through social cues in the eye region:

Oxytocin Improves “Mind-Reading” in Humans.

This “mind-reading” ability was measured using the Reading the Mind in the Eyes Test (RMET), which evaluates how well one can interpret emotions just by looking at photos of the eyes of different subjects.

You can take the quiz yourself here. Try it out. It’s pretty neat.

(I got 32.)

Oxtyocin therapy, although not necessarily addressing a root cause, may prove helpful as part of treatment for some autistics.

Note: It wouldn’t be too surprising if oxytocin levels were off in autistic individuals. Heavy metals, such as mercury, are suspected in the development of autism spectrum disorders. These metals concentrate in structures in the brain, such as the hypothalamus gland, pituitary gland, amygdala, and hippocampus, that help to regulate nearly every hormone in the body, emotions, learning, and memory.

From a recent US News & World Report cover story:

[P]erhaps as many as 640,000–under the age of 65…have dementia, the vicious thief of minds that steals memories, personality, relationships, language, and ultimately the ability to function as a human being.

“In the last five years, more younger people have been showing up at support group meetings and in doctors’ offices, asking for help, and we realized this is something we need to start taking seriously,” says neurologist Ronald Petersen, an Alzheimer’s and memory disorders specialist at the Mayo Clinic. It afflicts people in their 50s, their 40s, and even in their 30s. “Alzheimer’s is not just a disease that hits 80-year-olds in nursing homes,” says Dallas Anderson, a specialist in the epidemiology of dementia at the National Institute on Aging…

…”Nationally,” says Pierre Tariot, director of the Memory Disorders Clinic at the Banner Alzheimer’s Institute in Phoenix, “there’s not enough help for younger people with dementia–or older people.”

This growth in cases is clearly a significant challenge and a potential crisis, both in human and financial terms, if steps aren’t taken to proactively address it.

The official name for the early development of AD is “early-onset dementia.” The national Alzheimer’s Association acknowledged in a report earlier this year that it’s becoming a widespread problem:

Early Onset Dementia: A National Challenge, a Future Crisis

Younger afflicted individuals face complicated issues that older people don’t necessarily encounter:

In the years before they are diagnosed with the disease, younger people may fail at and lose their jobs, leaving their families in financial hardship and having to wait years before qualifying for disability or Social Security. After diagnosis, Schneider says, “friends and employers sometimes turn away from us, like they’re afraid they might catch the disease.”

The key questions are:

1. What is causing this increase in dementia cases among younger people?
2. What can be done to prevent the condition and/or slow its progression into AD?

Potential Causes

Regarding the first question, the answer is very complex, as there are likely multiple potential causes, both genetic and environmental. As noted in the US News article, however, the condition is likely more than genetics:

Scientists studying the genes of younger patients have found three mutations that seem to make some susceptible to the disease. But these genes don’t explain most of the cases, says John Morris, director of the Alzheimer’s Disease Research Center at Washington University in St. Louis.

What’s disappointing about the US News article is that it doesn’t emphasize the potential environmental factors, such as diet and environmental toxin exposure, that likely account for the majority of the increase in dementia cases.

Instead, the article paints a dire picture of a “progressive and incurable brain disease” that can currently primarily be treated with drugs that act as ineffective patches:

No one is truly happy with the current crop of drugs approved in the United States for the treatment of Alzheimer’s. Their names–Aricept, Cognex, Exelon, Razadyne, and Namenda–are familiar to anyone who cares for a dementia patient. “What all these drugs have in common is they act on the symptoms, not the underlying disease,” says John Morris, director of the Alzheimer’s Disease Research Center at Washington University in St. Louis. They boost chemicals that help the brain form memories, but “they don’t help a lot.”

The article does mention that new drugs are in development that may more directly address the condition. However, the drugs mentioned are focused on halting the development of beta-amyloid plaques. For years this area has been the primary focus of pharmaco AD research.

Now, though, the AD community is publicly acknowledging that there is likely much more to the picture. Many researchers have emphasized the importance of looking at potential upstream causes of plaque development, but have not gotten their ideas published. That focus may be changing, as this recent Wall Street Journal article noted:

[The] “there is more to” [AD than beta-amyloid plaques] statement. It is the focus of a paper in the October issue of the journal Alzheimer’s & Dementia reporting on a “research roundtable” convened by the private, nonprofit Alzheimer’s Association…

…[W]hen you think about it, concluding that B-amyloid and plaques cause Alzheimer’s is like believing a scab on your knee causes pain. The scab is the body’s response to an earlier injury. Similarly, there is evidence that amyloid plaques don’t cause Alzheimer’s.

To be fair, the online version of the US News article does include links to more about AD and potential treatments, and these links do mention the importance of pursuing diet and lifestyle habits that are good for the heart, as they are also likely helpful for brain health. But, the focus of the hardcopy article is on the drugs mentioned above, as well as on other palliative care steps, like using Post-It notes and computers to keep track of things.

Familiar Symptoms

It was interesting to read the story of one of the people with early-onset AD profiled in the article:

[H]e got weak and bedridden, sick with what turned out to be a wheat, or gluten, allergy. The next year, he was diagnosed with diabetes and started taking pills and insulin shots. But this was different. “My coordination and balance were off,” he says. “I had trouble hitting a light switch when I reached out for it. I found that I really had to concentrate on all my movements.” Over the next two years, memory troubles became more apparent…His major complaint is a lack of focus.

Wheat & gluten allergies? Poor blood sugar regulation? Coordination and balance problems? Progressive memory decline? Lack of focus?

And other AD symptoms from the US News story’s online resources:

• Problems with language.
• Disorientation and confusion.
• Inability to follow directions.
• Poor or decreased judgment.
• Problems with abstract thinking.
• Changes in mood and behavior.
• Changes in personality.
• Social withdrawal.

Gee, is there another condition with similar symptoms?

Hmmm, say one like…autism?

Could heavy metals, which are implicated in autism, also be playing a role in the development of dementia and Alzheimer’s disease?

Researchers have taken a look at the role of heavy metals in AD in a recent issue of the Journal of AD. Unfortunately, the focus of this research summary is on aluminum, iron, and metals other than mercury.

Yet, mercury poisoning symptoms closely mirror those of autism, mercury exposure produces brain lesions similar to those observed in AD, and mercury induces the formation of beta-amyloid and tau tangles (both commonly observed in AD) in neuroblastoma cells.

The question is: Why hasn’t more research been done to look at mercury as a potential contributory factor in the development of dementia and AD?

Could it be because the primary exposures to mercury are from amalgam fillings, vaccines, seafood, and emissions from coal power, chlorine, and cement plants? What role have interests representing these groups played in slowing and/or suppressing further research in this area?

What to Do

While we wait for answers to these questions, I think that anyone who is experiencing early-onset dementia would be making a big mistake to not explore whether heavy metals may be playing a role.

Unfortunately, there is no laboratory test for measuring heavy metals in the brain (if only it were so easy). Most doctors will run a blood or urine test to check for heavy metal poisoning. But knowledgeable practitioners know such tests are relatively worthless for measuring long-term, chronic exposure to heavy metals and current levels in various tissues of the body.

A hair test is the best bet for identifying potential heavy metal toxicities. And even this test, when done, is often interpreted incorrectly. (Hint: Low mercury levels don’t necessarily mean no toxicity. In fact, they could mean high toxicity.)

It’s important to work with someone who is familiar with:

• What test/s to run & how to correctly interpret them
• What to do if the test/s suggest metal toxicity, e.g.:
  • Safely remove existing exposures (e.g., amalgams)
  • Provide nutritional support
  • Safely reduce existing heavy metal levels using low, frequent-dose chelation.
  • Address existing chronic infections (e.g., fungal, viral)
  • Support endocrine function (thyroid, adrenals)

In my nutrition consulting practice, I am very familiar with this approach. In fact, I used it myself to fully recover from mercury poisoning and symptoms that, coincidentally, closely mirrored those of both autism and Alzheimer’s disease.

I was in my mid-30s when that occurred. The word “incurable” never entered my mind. If dementia begins to affect you or people you know, I hope that you won’t accept such a label and will instead work with a knowledgeable practitioner to take a close look as to whether heavy metal toxicity may be playing a role.

(Photos: Jeffrey MacMillan for US News & World Report)

New study (full text) out in the journal Archives of Internal Medicine that found that long-term supplementation of vitamin E in generally healthy older women did not significantly reduce the risk of cognitive decline.

But there may be more to the story.

Vitamin E is a powerful, fat-soluble antioxidant that helps to protect fatty substances in the body, such as cell membranes, nerve cells, lipoproteins, etc. Since oxidative stress is commonly observed in neurodegenerative diseases (e.g., Alzheimer’s) at even the earliest stages of the disease process, the thinking is that antioxidants such as vitamin E may help to reduce the onset and/or progression of the conditions.

There are actually eight forms of vitamin E: 4 tocopherols (alpha, beta, delta, gamma) and 4 tocotrienols (alpha, beta, delta, gamma). This study only used the alpha-tocopherol form of vitamin E. In earlier studies looking at vitamin E and cognitive decline, discussion regarding the type of vitamin E used has rarely been included. However, the authors of this study did raise this point (as did an editorial that accompanied the article):

It has been suggested that tocopherols such as {gamma}-tocopherol that is found in foods rather than in supplements* may be more important for delaying brain aging. Although {alpha}-tocopherol has stronger antioxidant properties, {gamma}-tocopherol has important additional anti-inflammatory effects that may enhance neuroprotection.

(* Broad-based vitamin E supplements containing gamma-tocopherol definitely are widely available. Well, at least the authors mentioned the issue.)

Also, recent research suggests that high amounts of alpha-tocopherol
may actually deplete gamma-tocopherol levels in the body. Given this potential, as well as gamma-tocopherol’s unique anti-inflammatory and antioxidant properties (e.g., its ability to inhibit cyclooxygenase and neutralize reactive nitrogen species — the latter especially relevant in protecting nervous system cells), it seems to make more sense to study the effects of a more balanced form of vitamin E on cognitive decline.

Other potential reasons why a beneficial result may have not been observed in this study:

• The dose given (600 IU, every other day) may have been too low.
• The supplements may not have been regularly taken with meals containing fat. Vitamin E is a fat-soluble vitamin and is not well absorbed unless taken with adequate amounts of fat.
• The timing of the initiation and length of the study may have been sub-optimal. Participants in this study were enrolled in their 60’s and given supplements for 10 years. Better results may have been observed if supplementation was started earlier in life and for a longer period.
• Approximately 1/4 of the study participants didn’t comply with the supplementation guidelines, and were thus excluded from the study results.

What would really be interesting to learn going forward is what neuroprotective effects may be offered by more balanced forms of vitamin E given to younger participants in moderate amounts and with meals containing fat. Such an interventional study would obviously take many years to perform in humans. Animal (e.g., mice) studies, although less conclusive, could be performed in the near-term.

Hopefully we’ll continue to see research done in this area, as early intervention is likely the best bet for heading off the progression of cognitive decline into more severe conditions such as Alzheimer’s disease.

A couple of more studies just released that again suggest omega fatty acids may be helpful in slowing cognitive decline:

Omega-3 fatty acid treatment in 174 patients with mild to moderate Alzheimer disease

This study found that patients with very mild Alzheimer’s disease (AD) who supplemented with omega-3 fatty acids (2.3 g/day)experienced significantly slower rates of decline in mental function. However, individuals with mild to moderate AD didn’t improve.

This result reinforces the importance of early intervention and prevention. Once damage to the brain is significant (as seen in moderate cases of AD), a single helpful nutrient like omega-3 fats, although not detrimental, is likely to not necessarily lead to great improvement.

Dietary supplementation of arachidonic and docosahexaenoic acids improves cognitive dysfunction.

Arachidonic acid is an omega-6 fat, while docosahexaenoic acid (or DHA) is an omega-3 fat. Most people get plenty of omega-6 fats in the diet, as they are found in high quantities in vegetable oils used in processed and restaurant-prepared foods. Arachidonic acid (ARA) is also found in high amounts in red meat and egg yolks. On the other hand, most people are deficient in omega-3 fats, such as DHA and eicosapentaenoic acid (EPA), which are found in fish oil.

This second study found that individuals with mild cognitive impairment who supplemented with only 240 mg of ARA and DHA experienced improvements in both immediate memory and attention scores. As in the earlier study, no improvement was seen in individuals who had already developed AD.

For omega-3 fats DHA & EPA, it’s important to make sure that the source (fish or supplements) is low in contaminants, such as heavy metals and PCBs. Tested fish oil supplements are your best bet there.

You can learn more about the important roles of omega-3 fats in disease prevention and treatment here.

And, you can learn more about ways to preserve and improve cognitive function here.

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.

Following up on yesterday’s post (Questioning the Usefulness of Nutritional Supplementation) that quotes Jeffrey Blumberg, professor of nutrition and director of the Antioxidants Research Laboratory at Tufts University, here’s an interesting recent interview with Professor Blumberg.

Some excerpts…

Current nutrition use in health care:

Something is terribly wrong. We know so much today about the “good” and “bad” fats and carbohydrates, nutrient density, caloric balance, glycemic load, and the role of micronutrients in promoting health, but we see a population that is carrying a burden of chronic disease that should be readily preventable by applying our current knowledge. It seems that our cornucopia of convenience foods and a lifestyle that has been engineered to make physical activity unnecessary have created a toxic environment that is very difficult to overcome.

As the key healthcare provider, the physician can and should play a major role in correcting this situation, but there is a regrettable lack of nutrition education and current nutrition knowledge among many physicians. There are, of course, other healthcare providers, including dieticians, nurses, and pharmacists, who can and should play a vital role in counseling and guiding their patients. But we face a fundamental problem that our whole healthcare system is still geared principally toward repair and recovery as opposed to health promotion and disease prevention.

This is where the real power of nutrition lies. We must treat patients with diabetes and heart disease and we must put pins in fractured osteoporotic hips, but we must not lose site of the fact that we must work harder to prevent these conditions in the first place. And the critical tools to doing so are nutrition and physical activity. There is a great deal of discussion regarding preventive medicine, but one need only review how medical care is insured and reimbursed to see how little recognition is granted to the value of health promotion…

…It is helpful to appreciate that much of health promotion is directed to reducing the risk or delaying the onset of age-related chronic diseases. But mainstream medicine is still too focused on treating these conditions after they have become manifest instead of preventing them. Nonetheless, there are a growing number of integrative clinicians who are adopting diet and nutrition as one of the mainstays of their practice. There is certainly a segment of practicing dietitians as well that are strong advocates for health promotion through diet and the use of supplements, but many are based in hospitals and directed to nutritional support of patients.

Nutrient needs at all ages:

We need to appreciate that there are lifecycles for nutrient requirements, and one of those cycles includes older adults and the elderly. Of course, aging does not begin at 50 or any other single age but is segmented by physiological systems. For example, immunological reserves begin to decline with the involution of the thymus at puberty, reduction of bone mineral density occurs in the middle of our fourth decade, and loss of lean body mass (sarcopenia) becomes apparent when we’re in our 60s.

Elderly nutrient needs:

When dealing directly with the elderly, we find a marked increase in nutrient inadequacies for many reasons, including a lack of attention to nutrient density, no use or misuse of supplements, and drug-induced nutrient deficiencies. Importantly, in contrast to earlier beliefs that because older people are smaller and more sedentary they have lower nutrient needs, we now know that the requirements for several nutrients increase with age.

The increased requirement for many nutrients with age often translates into the rational application of dietary supplements.

Drug-nutrient interactions:

One other thing that I would stress is that older people as a group take more medications more frequently and for longer periods of time than any other age group. And yet we know there are many drug-induced nutritional deficiencies. This is a problem that is significantly underappreciated and that often goes unrecognized despite the simple solution available to prevent it.

The medical establishment’s understanding and acceptance of supplement research and supplements in general:

[E]ven when there are successes with supplement trials—and there certainly have been several—there seems to be reluctance to adapt the actual evidence to practice. For example, when folic acid supplements were proven to reduce neural tube birth defects or when supplements of marine omega-3 fatty acids were shown to lower the risk of cardiovascular disease, the strongest recommendations were to eat more vegetables and fish, respectively, even though the trials were conducted with supplements. Similarly, the dramatic reduction in fractures obtained with calcium and vitamin D supplements resulted largely in the recommendation for greater consumption of dairy products, not of the supplements with demonstrated efficacy…

…Perhaps many physicians do not feel knowledgeable enough about nutrition to make the recommendation, or they simply do not have the time to assess each patient’s dietary pattern and nutritional status. This only suggests to me the need for a healthcare team approach, actively involving dietitians and pharmacists to contribute to this effort.

Evidence-based medicine:

[W]e are required to use our best medical and scientific judgment on the totality of available evidence, including basic research and observational studies as well as clinical trials, and reach conclusions today about what to recommend as food choices and supplement use. Why would we want to ignore the data derived from in vitro and cell culture experiments, animal models, case reports, population-based studies, and millennia of traditional medical and dietary practices and presume that a single research approach, randomized clinical trials, is the only way we can come to know about the value of nutritional interventions? Holding out for this single “gold standard” is not only too limiting to a full understanding of nutrition but holds out the false promise that all the necessary trials will be done in our lifetime or even in our grandchildren’s lifetimes.

Check out the entire interview. It’s well worth the time.