Marc Joseph Nutrition - Blog

In a review study published in the journal Thrombosis and Hemostasis, researchers note that vitamin K deficiency may be much more common than previously thought.

A primary action of vitamin K in the body is to help in a chemical reaction called carboxylation. Potential vitamin K deficiencies can be identified by measuring in the body the level of under-carboxylated compounds, such as osteocalcin and matrix Gla protein (MGP), both of which are involved in the maintenance of bone structure.

The scientists note that there is a substantial amount of incompletely metabolized osteocalcin and MGP in many otherwise apparently healthy individuals, which suggests that the majority of these people may be subclinically deficient in vitamin K.

Results Not Surprising

The findings aren’t too surprising, given that the primary dietary sources of vitamin K are:

• Green, leafy vegetables - spinach, kale, chard, lettuce
• Broccoli
• Parsley

These aren’t foods that most people eat regularly in adequate amounts (e.g., a cup per day). And, the biological half-life of vitamin K is relatively short — a few days. That means if you’re not regularly consuming vitamin K, you may become deficient.

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In a five-year study published in the top journal Neurology, researchers found that individuals who developed mild cognitive impairment (MCI) or Alzheimer’s disease had observable changes in brain structure long before the onset of cognitive decline.

Compared to the group that didn’t develop memory problems, the 23 people who developed MCI or Alzheimer’s disease had less gray matter in key memory processing areas of their brains even at the beginning of the study when they were cognitively normal.

“We found that changes in brain structure are present in clinically normal people an average of four years before MCI diagnosis,” said study author Charles D. Smith, MD, with the University of Kentucky Medical Center in Lexington and member of the American Academy of Neurology. “We knew that people with MCI or Alzheimer’s disease had less brain volume, but before now we didn’t know if these brain structure changes existed, and to what degree, before memory loss begins.”

The findings are definitely interesting, but not too surprising. As shown in the video below, it is known that exposing nerve cells to toxins may lead to damage consistent with that observed in Alzheimer’s disease:

How Mercury causes Neurodegeneration (brain degeneration)

Toxin exposure is, of course, not the only potential cause of cognitive decline. Nutritional deficiencies, stress, genetics, and other factors may also be involved.

Waiting Not a Good Option

As someone who experienced and recovered from MCI at a relatively young age, I can’t emphasize enough the importance of not ignoring minor cognitive changes (e.g., ability to think, focus, remember). MCI and Alzheimer’s disease are NOT a normal part of aging.

Each person has an internal reference point to their own cognitive abilities and usually is capable of recognizing changes in function long before friends, family, and co-workers may be aware there is an issue. It’s important to be self-aware and try to compare your current capabilities with where they’ve been and where you’d like them to be.

As this study suggests, if you suspect a decline in cognitive function, the time to act is now, as such change may be preceded by years of structural changes.

There are many preventive and therapeutic steps that may help prevent, slow, and possibly even help to reverse the development of conditions like MCI and AD. You can read an overview of my approach to helping people here. Diet, supplementation, lifestyle changes, and in some cases, low/frequent-dose chelation, may each play a role.

Cognitive decline is not inevitable. Don’t believe anyone who says it is.

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Discover How Nutrition Can Make a Difference in Your Life …

Marc Joseph Nutrition

In a study published in the journal Diabetes, researchers found that increased belly fat led to the production by fat cells of higher levels of inflammatory molecules that may directly promote systemic (whole body) inflammation. This increase in systemic inflammation may, in turn, raise the risk for several diseases, such as heart disease, diabetes, cancer, and cognitive decline.

There are two types of abdominal fat:

1. Subcutaneous fat - found just beneath the surface of the skin (the fat you can “pinch”)
2. Visceral fat - found in the spaces between internal organs

(Image: LA Times)

Visceral fat appears to be the primary source of the problem:

[T]he research team says visceral fat likely contributes to increases in systemic inflammation and insulin resistance. They sampled blood from the portal vein [which routes blood to the liver from the gastrointestinal tract] in obese patients undergoing gastric bypass surgery and found that visceral fat in the abdomen was secreting high levels of an important inflammatory molecule called interleukin-6 (IL-6) into portal vein blood.

“The portal vein is filled with blood that drains visceral fat,” says first author Luigi Fontana, M.D., Ph.D., assistant professor of medicine at Washington University in St. Louis and an investigator at the Istituto Superiore di Sanita, Rome, Italy. “Portal vein blood had levels of IL-6 that were 50 percent higher than blood from the periphery.”

Increased IL-6 levels in the portal vein correlated with concentrations of an inflammatory substance called C-reactive protein (CRP) in the body. High CRP levels are related to inflammation, and chronic inflammation is associated with insulin resistance, hypertension, type 2 diabetes and atherosclerosis, among other things …

… “Many years ago, atherosclerosis was thought to be related to lipids and to the excessive deposit of cholesterol in the arteries,” Fontana says. “Nowadays, it’s clear that atherosclerosis is an inflammatory disease. There also is evidence that inflammation plays a role in cancer, and there is even evidence that it plays a role in aging. Someday we may learn that visceral fat is involved in those things, too.”

Evidence Building

This latest study is one of many to highlight the influence of excess fat on systemic inflammation and disease risk. Here are links to a few other studies:

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Methylation, the donation of methyl (CH3) molecules, is a primary mechanism by which genes in a cell’s DNA are turned off. Lack of methyl groups or removal of methyl groups (demethylation) causes genes to remain or become activated.

In a process called epigenetics, cells also use methylation to specialize later in development without relying upon the instructions contained in the cell’s DNA. This type of specialization is especially vulnerable to environmental factors, such as nutritional deficiencies and exposure to toxins.

In a recent study published in the journal Neuron, researchers suggest that this type of epigenetic methylation may be key in forming memories.

In their experiments, the researchers conditioned fearful memories in rats by giving the animals mild shocks when they were in a specific training chamber. The researchers could then test whether the rats remembered the conditioning by observing whether they froze when placed in the chamber.

Using drugs that inhibit methylation, the researchers showed that methylation was necessary for rats to form such memories. Particularly importantly, the researchers found that the level of methylation directly controlled the activity of genes known to either suppress or promote memory formation. The memory suppressor gene they studied is called protein phosphatase 1, and the memory-promoting gene is called reelin.

“To our knowledge, this study is the first to present evidence that DNA methylation, once thought to be a static process after cellular differentiation, is not only dynamically regulated in the adult nervous system but also plays an integral role in memory formation,” concluded Miller and Sweatt. They wrote that their findings indicate that DNA methylation has been co-opted by the central nervous system as a “crucial step” in regulating gene activity involved in memory formation.

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Last month, I had a post discussing the importance of ensuring adequate levels of both folic acid and vitamin B12 to help prevent cognitive decline:

Key Nutrients in Helping to Prevent Cognitive Decline

In a new study out this month in the American Journal of Clinical Nutrition, researchers evaluated 1779 Mexican Americans between the ages of 60 and 101, and found that those individuals with high homocysteine levels and low vitamin B12 levels were at significantly greater risk of developing dementia.

Specifically, study participants with high homocysteine levels had more than double (139%) the risk of developing dementia than individuals with normal homocysteine values. And, participants whose serum vitamin B12 levels were in the lowest third of those measured had more than 60 percent greater risk of dementia.

Vitamin B12 is used in the primary pathway conversion of homocysteine back to methionine in the methylation cycle. (Betaine, or tri-methyl-glycine, is used in the secondary pathway converting homocysteine to methionine.) Methylation reactions are fundamental to many cellular processes, including expression of genes and proteins. Without adequate vitamin B12 intake, absorption, and utilization, homocysteine levels rise and the methylation cycle is impaired.

Vitamin B12 is also critically important in the methylation reactions involved in the proper formation of myelin, the “insulation” that coats nerve cells and is necessary for proper communication between them.

An interesting note about this study is that the researchers found a significant negative relationship between vitamin B12 and dementia (low vitamin B12, high dementia risk) looking only at serum vitamin B12 levels. That’s certainly one measure of potential deficiency, but a more reliable approach would be to measure methylmalonic acid (MMA), which builds up when vitamin B12 is low and is a sensitive, early deficiency marker. Your best bet for assessing vitamin B12 deficiency is to look at serum vitamin B12, MMA, and homocysteine levels in aggregate, rather than just relying on one measure.

Vitamin deficiencies (e.g., vitamin B12, folate) may be involved in dementia and cognitive decline, but they are not the only potential causes. For more on other contributing factors, see here.

In a recent epidemiological study of rural Chinese seniors, researchers found that lower selenium levels in nail samples were associated with lower cognitive scores.

Specifically, researchers observed that people in the group with the 20% lowest selenium levels scored 10 years older on a standardized cognitive test than people with the 20% highest selenium levels.

Selenium is an essential trace mineral — meaning you only need very small amounts of it (micrograms - mcgs, or millionths of a gram) and have to get it from your diet or through supplements. Selenium may also be toxic in higher amounts (e.g., more than 400 mcg/day), so this is a case where a lot more is not better.

The mineral plays very important roles in the body, such as inclusion in key enzymes:

• Glutathione peroxidases, which help one of the body’s primary antioxidants (glutathione) to neutralize free radical molecules.
• Thyroid hormone deiodinases, which help convert inactive thyroid hormone T4 into the biologically active form T3, among other functions.

Selenium may help to reduce the risk of certain cancers (e.g., prostate, colon), improve immune function, and lower the risk of cardiovascular disease (via reduced oxidative damage to the arterial walls). Also, selenium appears to sequester, although not chelate, mercury.

Brazil nuts are the food highest in selenium (potentially > 100 mcg per nut, depending on the soil). Organ meats and seafood are also high in selenium. Selenium levels in grains and plant foods can vary greatly depending on the soil in which they are grown. Here’s an (old) map that shows soil selenium levels in North America.

As the authors of the study above note, it’s important to realize that the effects of selenium deficiency likely occur over a long period. Selenium supplementation is not a quick fix. Including a reasonable amount of selenium (e.g, 200 mcg/day) in a well-utilized form (e.g., selenomethionine) as part of a preventive program started well before cognitive decline symptoms appear makes the most sense.

In a recent study published in the British Medical Journal, researchers found that children with high IQs were significantly more likely to become vegetarians as adults.

The study looked at over 8,000 adults born in 1970 and who had their IQs measured at age 10 as part of another study. 366 of the study participants identified themselves as vegetarians by age 30. Vegetarians had, on average, an IQ 5 points higher than non-vegetarians (and that was after adjusting for gender, social class, and education).

123 of the self-identified vegetarians also ate chicken or fish, which meant they weren’t actually vegetarians. But even after excluding these individuals, the study’s results remained unchanged.

A vegetarian diet is certainly not the only healthy dietary approach for helping to ensure optimal cognitive function. For people whose ancestors ate a diet higher in meat and dairy, a diet that includes some animal products may work better with their own biochemistry.

However, a vegetarian diet, if constructed to ensure the inclusion of key nutrients that may be lacking (e.g., protein, vitamin B12, calcium, zinc, iron, omega-3 fats, etc.), is certainly a viable approach.

There is a significant amount of research that suggests a vegetarian diet may help to:

• Improve cholesterol levels
• Decrease blood pressure
• Reduce the risk of developing:
  • hypertension
  • cardiovascular disease
  • type 2 diabetes
  • certain cancers (e.g., colon, prostate, breast)
  • dementia
• And more …

No guarantees that a vegetarian diet will help to make you smarter, but it may help to make you a little healthier.

Vitamin B12 is a critical nutrient in helping to maintain cognitive function, as one of its primary roles is to aid in the formation of myelin, the insulation that lines nerve cells, such as brain cells. It’s also a key nutrient in a process called methylation, which helps control the expression of genes and proteins that are involved in many important chemical pathways in the body. An imbalance in methylation may also play a role in cancer development.

Deficiency of vitamin B12 is most commonly observed in older adults, partly because of dietary changes (less meat intake), but also as the result of impaired absorption. When foods containing vitamin B12 (e.g., meat) are eaten, intrinsic factor, a substance secreted by cells in the stomach, binds to vitamin B12. That compound travels to the end of the small intestine, where it separates and vitamin B12 is absorbed. If for some reason the stomach or gastrointestinal tract is damaged (e.g., as in atrophic gastritis) or stomach acid production is slowed (e.g., with medications such as proton pump inhibitors), this multi-step absorption process may be interrupted.

Once vitamin B12 is absorbed, utilization in the body and methylation pathways may also be impaired by the presence of heavy metals, such as mercury, lead, and aluminum.

Several laboratory measures are used together (by thorough practitioners) to test for vitamin B12 deficiency, including:

• Serum vitamin B12
• Methylmalonic acid (MMA)
• Homocysteine

In a recent paper published in the American Journal of Clinical Nutrition, researchers found that high MMA values (suggestive of vitamin B12 deficiency) were associated with significantly lower scores on a standard cognitive assessment tool, especially in the areas of language comprehension and expression.

Low serum folic acid levels also were associated with poorer cognitive function scores. Folic acid, along with vitamin B12, is essential in the proper functioning of methylation pathways, which often are not working correctly in conditions such as cognitive decline, autism, and ADD/ADHD.

Lest you think that these deficiencies only affect a small percentage of people, 43 percent of the non-demented individuals age 69 and older in the study had MMA values that suggested significant vitamin B12 deficiency.

It’s critically important to make sure that both vitamin B12 and folate levels are maintained at adequate levels to reduce the risk of cognitive decline. You can learn more about treatment approaches for preventing and slowing cognitive decline here.

With many baby boomers about to retire, maintaining independence and the ability to live an active, engaged retirement are top of mind. A recent study published in the Archives of Internal Medicine found that deficiencies in several micronutrients may increase the risk for having difficulty performing daily tasks as people age.

Specifically, the study looked at women over the age of 65 and found that deficiencies in selenium, vitamin B6, and vitamin B12 were all associated with significantly greater risk of experiencing disability, which was defined as self-reported difficulty in performing two or more activities such as bathing, dressing, toileting, transferring and eating.

Selenium is an essential trace mineral that is used by the body in important antioxidant-related enzymes. Selenium also plays an important role in immune function and may help to prevent the onset of certain cancers, such as prostate cancer.

Vitamin B6 and B12 are involved in important enzyme reactions, nervous system function, and help to maintain low homocysteine levels. High homocysteine levels are associated with oxidative stress, endothelial dysfunction, vascular diseases (heart disease, stroke), and, in particular, with decline of cognitive function.

Nutritionally, your best bet for avoiding the potential problems highlighted by this study are to follow a good diet, including mostly whole foods, lots of fresh vegetables & fruits, healthy fats, and lean protein sources.

Also, supplementation with a broad-based multi-vitamin/mineral containing at least 200 mcg selenium and the B vitamin equivalent of a B-50 complex, may help to ensure that you get adequate amounts of these essential nutrients on a regular basis and to prevent/delay the onset of disability. It’s important to select supplements containing both adequate and well-absorbed forms of the different nutrients.

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.