Gerardin 2012

You have likely heard the headlines: cognitive impairment and Alzheimer’s and other forms of dementia are on the rise. Part of the increase is due to an aging population. But there are reasons that are adding to the increase beyond this. The epidemics of insulin resistance (recall that dementia is often labeled “type 3 diabetes,” meaning that the brain becomes insulin resistant), SIBO endotoxemia, the ubiquity of heavy metal toxicity, and deficiencies of important nutrients such as omega-3 fatty acids and vitamin D are likely making their own contributions.

There are a number of strategies that you can adopt, however, that hold potential for reducing your risk for developing cognitive impairment, or at least delay its onset. (In my Inner Circle, for instance, we have spent the last couple of weeks discussing the value of cognitive and physical exercise.) There are also various factors that you can supplement, some of which hold potential for improving cognition and, in some cases, slow or help prevent cognitive impairment and dementia. But this area is filled with imprecise thinking and, sadly, misleading marketing. To help you get your arms around these ideas, let me introduce you to a concept that makes gaining an understanding of what works and what doesn’t that can keep you on track and avoid pitfalls that waste time, effort, money, and have little to no benefit for brain health.

In the world of factors that you can supplement for brain health, there are two distinct categories:

Nootropics—These are agents that make you more creative, better able to recall or commit to memory, increase attention, improve your ability to synthesize new ideas. In short, nootropics make you a little smarter—for a few hours. But then the effect is gone and brain health is no better nor worse. Nootropics work by increasing the levels of neurotransmitters such as acetylcholine, dopamine, and norepinephrine. But most nootropics have no impact on the pathologies associated with cognitive decline such as accumulation of β-amyloid plaque, tau protein (the two factors that accumulate in the brains of people with dementia), the progression of cerebral and hippocampal atrophy, no effect on increasing “trophic” hormones that preserve brain health such as brain-derived neurotrophic factor (BDNF), IGF-1α, or vascular endothelial growth factor (VEGF).

The world of nootropics includes a long list of agents that I’ll bet most of you never heard of, agents such as huperzine, citicoline, dimethylaminoethanol, piracetam, bacopa monnieri, selegiline, ergyloid mesylates, and (my favorite) vinpocetine. (It’s my favorite because it yields a soft boost in creativity and focus with no adverse effects.) Caffeine is a weak nootropic—remember the first few cups of coffee you had? You were more energetic, attentive, focused, and more creative. But the effects wear off just a few hours later—is your brain any healthier now? No, of course not. Caffeine is an example of a mild nootropic. By the way, prescription drugs for dementia such as memantine, donepizil, rivastigmine and others are nootropics (lousy nootropics at that)—they improve mental function slightly but do not slow the progression of the disease. Numerous scam products that are widely advertised also claim to improve brain health because they may improve some aspect of mental function but, in reality, have no impact on the development of dementia. In other words, improved cognitive performance is not the same as improved brain health and prevention of cognitive impairment. There may be an occasional nootropic that also provides benefits on brain anatomy and physiology, i.e., exerts some degree of neurotrophic effect, but the evidence for this is meager to non-existent.

Neurotrophics—Neurotrophics, on the other hands, are agents or practices that improve brain anatomy or physiology, not just transient cognitive performance. As I mentioned above, improvements in brain health could include:

  • Reduced brain accumulation of β-amyloid plaque and/or tau protein
  • Increased trophic factors that promote brain cell reproduction, increased brain cell interconnections (synapses), healthier supportive glial cells and other factors. Increases in BDNF, IGF-1α and VEGF in the brain are reflected by increased blood levels of these factors, also.
  • Reduced atrophy of key brain areas—especially the hippocampus, the part of the brain that converts short-term to long-term memory, the cerebral cortex, temporal lobe and other brain structures.

The list of neurotrophic factors that hold potential to slow or halt cognitive decline and thereby dementia is a shorter list than the list of nootropics. But among the most important are:

  • Omega-3 fatty acids—especially DHA, as brain matter is largely made of DHA.
  • Vitamin D—and other factors such as magnesium that minimize insulin resistance.
  • Follow a diet that does not lead to insulin resistance or protein glycation—Elimination of wheat, grains, and sugars are magnificently effective at this, while low-fat diets are not. Reducing insulin resistance cascades into other beneficial brain effects that result from reduction of abdominal visceral fat and thereby inflammation.
  • Physical exercise—that has been shown to increase BDNF, increase hippocampal volume, in addition to yielding cognitive benefits. This is in distinction to cognitive exercises such as doing crossword puzzles, Sudoku, learning a new language or musical instrument, activities that improve your ability to do, for instance, Sudoku, but likely have no meaningful effects such as reduced β-amyloid plaque or increased BDNF (though the evidence is somewhat muddled here).
  • Reduced endotoxemia—While the evidence is preliminary, addressing endotoxemia, especially that associated with small intestinal bacterial overgrowth (SIBO), is looking like a major factor that can be addressed. Endotoxemia stimulates production of β-amyloid plaque, provokes insulin resistance and inflammation, and has been associated with atrophy of brain structures. We, of course, have been normalizing breath hydrogen gas (as measured by the AIRE device) with my recipe for SIBO Yogurt.

The effects of SIBO Yogurt, or at least restoration of the microbe lost by most modern people, L. reuteri, may provide additional neurotrophic benefits that develop from the increase in oxytocin that blunts rises in cortisol (that is neurotoxic), testosterone (thereby reducing abdominal visceral fat), the restoration of youthful skeletal muscle and thereby growth hormone, and the generally brighter emotional and social outlook it provides.

There are a handful of other factors that may provide neurotrophic benefits, most of which are based on preliminary (animal, observational) evidence. But know that, by addressing the above factors/strategies with beneficial neurotrophic effects, you have gained significant advantage in preserving cognitive health. It also means ignoring the misleading and over-the-top claims of this or that “brain” or “memory” supplement and avoiding the generally useless strategies introduced should you have the misfortune of having to check into the assisted living or memory center.