{"id":587,"date":"2017-06-19T06:00:31","date_gmt":"2017-06-19T06:00:31","guid":{"rendered":"http:\/\/joshmitteldorf.peachpuff-wolverine-566518.hostingersite.com\/?p=587"},"modified":"2017-06-19T06:00:31","modified_gmt":"2017-06-19T06:00:31","slug":"preventing-dementia","status":"publish","type":"post","link":"https:\/\/scienceblog.com\/joshmitteldorf\/2017\/06\/19\/preventing-dementia\/","title":{"rendered":"Preventing Dementia"},"content":{"rendered":"

Abating Risk of AD<\/b><\/p>\n

Dementia seems to appear out of nowhere. \u00a0People feel like helpless victims of their genes. \u00a0But this is a misconception. \u00a0How much does the dreaded ApoE4 gene increase your chance of getting dementia? \u00a0This is not a straightforward calculation precisely because the correlation must be controlled for many diet and lifestyle factors that are proving to be just as important as genetics. \u00a0For women with ApoE4 from one parent, risk of AD is doubled, but this factor is easily reclaimed with diet, exercise and supplements. \u00a0For men, the effect of one copy of ApoE4 is small enough to be lost in the noise. \u00a0<\/span><\/em>For men and women with two copies of ApoE4, risk of AD is very high, but even here factors under your control offer hopeful remediation.<\/span><\/em><\/p>\n

I confess that I love public attention. \u00a0<\/span><\/em>For a long time, I thought of this as a personal failing, and consciously avoided pursuing publicity. \u00a0When I came up with radical notions about evolutionary biology and the direction of medical research, I counted on people to think for themselves and evaluate the evidence; if they looked only at the credentials of the theorist, I was seriously outgunned. <\/span><\/p>\n

Reputation <\/span>shouldn\u2019t<\/span><\/i> matter, but it does \u00a0<\/span>Only in the last decade, I have come to realize that people are receptive to ideas from those they already trust, and skeptical of ideas that come from an unknown source. I\u2019m learning to burnish my reputation\u2026<\/span><\/p>\n

So when I got an inquiry from a CBS news intern asking \u201cWhat can we do to improve our odds of avoiding dementia?\u201d, I set aside time to review the literature before I talked to him. \u00a0Here\u2019s what I found.<\/span><\/p>\n

 <\/p>\n

Exercise is most important<\/b><\/p>\n

Five areas that I investigated are:<\/span><\/p>\n

    \n
  1. Physical exercise<\/span><\/li>\n
  2. Mental stimulation and social factors<\/span><\/li>\n
  3. Metabolic syndrome \/ insulin sensitivity<\/span><\/li>\n
  4. Diet<\/span><\/li>\n
  5. Brain-targeted drugs and supplements<\/span><\/li>\n<\/ol>\n

    As I set out on my quest, I was prepared to find that #2 was the most important. \u00a0For longevity, social connections are more important than anything else; and I reasoned that for keeping the brain healthy in late life, this should be even more true. \u00a0But I was surprised. \u00a0#2, mental stimulation and social factors are effective in <\/span>some studies<\/span><\/a> but not <\/span>others<\/span><\/a>. \u00a0The clear winner in the literature is #1. \u00a0There is <\/span>robust evidence<\/span><\/a> that physical exercise lowers your risk of dementia. \u00a0Here\u2019s a meta-analysis from <\/span>2011<\/span><\/a> and a review from <\/span>2017<\/span><\/a>. \u00a0Modest amounts of exercise are way better than being a couch potato. \u00a0There is some extra benefit from being a gym rat, but there are diminishing returns with intensity.<\/span><\/p>\n

    <\/p>\n

    Social connection and intellectual stimulation<\/b><\/p>\n

    The most positive study connecting social factors with a slowing of cognitive decline was in <\/span>2001<\/span><\/a>. \u00a0A team from UCLA followed 1200 men and women over 7.5 years, and concluded that, among social factors, \u201cemotional support\u201d was the most important factor.<\/span><\/p>\n

    But in subsequent studies, the importance of emotional support faded. \u00a0In a review in <\/span>2010<\/span><\/a>, no social variables made the list of protective factors. \u00a0And this <\/span>2016<\/span><\/a> study found social connectivity to be connected to base levels<\/em> of cognitive function at midlife but not to 20-year change<\/em> in cognitive performance.<\/span><\/p>\n

     <\/p>\n

    The MIND diet<\/b><\/p>\n

    Of several diets that have been tested for neuroprotective benefit, the <\/span>MIND diet<\/span><\/a>, developed by Martha Morris of Rush University in Chicago seems to be the best documented. \u00a0In the only test so far, Morris claims it can cut AD risk by 50%. \u00a0The M in MIND is for <\/span>Mediterranean<\/span><\/a>, of which the MIND diet is a variant. \u00a0Start with lots of leafy greens, berries and nuts, fruits and vegetables, olive oil, whole grains and fish for protein and omega 3s. \u00a0The MIND variant emphasizes blueberries and walnuts, which seem especially good for the brain. [<\/span>Details at WebMD<\/span><\/a>]<\/span><\/p>\n

    <\/p>\n

    Habitual coffee drinking is associated with a modest decrease in risk [<\/span>2016<\/span><\/a>], but tea, especially green tea is better [2015<\/a>]. \u00a0\u00a0This study [<\/span>2006<\/span><\/a>] found a factor of 2 benefit for the heaviest tea drinkers in Japan. \u00a0Caffeine seems to be moderately neuroprotective [<\/span>2008<\/span><\/a>], but the best benefit comes from catechins=polyphenols, for which decaf tea works as well.) \u00a0Green tea is part of the MIND diet.<\/span><\/p>\n

     <\/p>\n

    Metabolic Syndrome<\/b><\/p>\n

    Beginning 20 years ago, a strong association was found between metabolic syndrome and AD [<\/span>1997<\/span><\/a>]. \u00a0Insulin treatments seemed to worsen the risk [<\/span>1999<\/span><\/a>] — indeed, excessive insulin seems to be at the heart of the connection. \u00a0Some people started saying we should think of AD as <\/span>type 3 diabetes<\/span><\/a>. \u00a0Metformin is the standard treatment for diabetes, and this study [<\/span>2011<\/span><\/a>] found that taking metformin brought the risk of AD in diabetics back down to a rate comparable with age-matched non-diabetics. \u00a0But this study [<\/span>2013<\/span><\/a>] found that taking metformin actually <\/span>increases <\/span><\/i>risk of AD. \u00a0A strong hypothesis is that metformin uses up vitamin B12. \u00a0B12 is essential for functioning of neurons, and is concentrated in the brain. \u00a0Many people are deficient in B12 even without metformin, and anyone taking metformin should be supplementing with B12. \u00a0Whether there is residual risk of AD from metformin even with B12 remains to be seen, but probably it\u2019s not just people on metformin who should be supplementing with B12 [<\/span>2014<\/span><\/a>, <\/span>2015<\/span><\/a>]. \u00a0Low protein diets are protective for many aspects of aging, and the MIND diet is mostly vegetarian. \u00a0B12 is one essential nutrient that can’t be derived from vegetable sources.<\/span><\/p>\n

     <\/p>\n

    Drugs, Hormones and Supplements<\/b><\/p>\n

    The most common pharmaceutical approach is to enhance the neurotransmitter acetylcholine. \u00a0Acetylcholine is found wherever nerves are found, for cognition, sensation and motor control, and it seems especially imortant for memory. \u00a0\u00a0Alpha GPC (glyceryl phosphoryl choline) is an acetylcholine precursor which can be taken orally. \u00a0In this study [<\/span>2003<\/span><\/a>], 132 AD patients taking Alpha-GPC tested better after 90 and 180 days than at the outset, compared to worsening in those taking placebo. \u00a0Whether A-GPC is nootropic or neuroprotective is less clear. \u00a0Here is a <\/span>bibliography from Examine.com<\/span><\/a>. <\/span><\/p>\n

    I\u2019ve been slow to recognize the potential of angiotensin receptor blockers (ARBs), prescription drugs which seem to be a new class of age-slowing drugs which I have not discussed previously. \u00a0The best known is Losartan. This study [<\/span>2010<\/span><\/a>] found a 25% reduction in AD. \u00a0And in studies with rats, ARBs increase lifespan [<\/span>2009<\/span><\/a>]. \u00a0They work by relaxing the arteries, lowering blood pressure, relieving in the process the risk of all cardiovascular diseases. \u00a0The trouble with ARBs is that people don\u2019t like them. \u00a0Some people feel lethargic, weak and unmotivated. \u00a0Some people cough. <\/span>\u00a0<\/span>Telmisartan<\/span><\/a> is supposed to be the drug in this class with the least side effects.<\/span><\/p>\n

    Both male and female sex hormones are protective against dementia [<\/span>2017<\/span><\/a>]. \u00a0A modest way to get this benefit without taking sex hormones is by supplementing with DHEA. \u00a0DHEA levels decline with age, and serum <\/span>DHEA is lower in AD patients<\/span><\/a>, suggesting but not proving that DHEA might be protective.<\/span><\/p>\n

    Pregnenolone<\/span><\/a> is another hormone precursor, and in fact the body makes DHEA from pregnenolone. \u00a0As with DHEA, we have less pregnenolone as we get older. \u00a0Studies with mice have found pregnenolone leads to increased memory retention in the here and now. \u00a0Evidence that it is neuroprotective is lacking.<\/span><\/p>\n

    Poor sleep quality, sleeping more than 8 or less than 7 hours per night, and sleep apnea are all risk factors for dementia [<\/span>2016<\/span><\/a>]. \u00a0The effect is large, but the data is thin. \u00a0Sleep is commonly disrupted in AD, with melatonin levels that are low and not synched to the circadian cycle. \u00a0Melatonin supplementation is a natural thing to try, and there has been some limited success with melatonin as a treatment for AD [<\/span>2010 review<\/span><\/a>]. \u00a0I found no data on whether it helps as a preventive, but sleep-inducing pharmaceutical alternatives are associated with increased<\/em> risk.<\/span><\/p>\n

     <\/p>\n

    Honorable mention<\/b><\/p>\n

    These supplements are reported to be neuroprotective or nootropic or both. \u00a0It\u2019s interesting to me that there is an overlap. \u00a0We don\u2019t have to choose \u201cnow or later\u201d, but can have our cake and eat it, too.<\/span><\/p>\n\n\n\n\n
    Primarily nootropic<\/strong><\/td>\nPrimarily neuroprotective<\/strong><\/td>\n<\/tr>\n
    Bacopa<\/span><\/a>
    \n    Ginkgo biloba<\/span><\/a>
    \n    Ginseng<\/span><\/a>
    \n    Gotu kola<\/span><\/a>
    \n    Huperzine<\/span><\/a>
    \n    Piracetam<\/span>
    \n<\/span><\/a>    Lion\u2019s Mane Mushroom<\/span><\/a><\/td>\n    		Acetyl L-Carnitine<\/span><\/a>
    \n    Ashwagandha<\/span><\/a>
    \n    Nigella sativa<\/span><\/a> (=kalonji=charnoucha)<\/span>
    \n    Curcumin<\/span><\/a> (turmeric)<\/span>
    \n    Ginger<\/span><\/a>
    \n    Omega 3 fatty acids<\/span><\/a>
    \n    Alpha lipoic acid<\/span><\/a><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n


    \nHope for the doubly unlucky<\/b><\/p>\n

    One person in 50 has two copies of the ApoE4 gene<\/a>. \u00a0Age-adjusted risk of dementia is more than 10 times higher for both male and female. \u00a0For these folks, there is a theory [1989<\/a>] that keeping blood cholesterol low can completely ameliorate the risk. \u00a0The theory comes from a mechanistic analysis and extrapolates from the odd fact that Nigeria has the highest prevalence of ApoE4 in the world, but there is no elevation of dementia. \u00a0More recent [2016<\/a>] is speculation that ApoE4 carriers need much more omega 3 than the rest of us.<\/p>\n

    My favorite Alzheimer\u2019s study<\/a> comes from Dale Bredesen at Buck Institute [2014<\/a>], who offered intensely personalized treatment protocols to ten Alzheimer\u2019s patients, and dramatically improved cognitive performance for 9 of the 10. \u00a0This is a stunning example demonstrating what medical science is capable of when institutional barriers are removed and clinicians have time to work with patients individually.<\/p>\n

    Dale Bredesen<\/figcaption><\/figure>\n

    Bredesen\u2019s work offers incidentally the hopeful possibility that the benefits of some of the measures I have described are cumulative, and that with carefully crafted individual programs they can be combined to push Alzheimer\u2019s risk back many years.<\/p>\n","protected":false},"excerpt":{"rendered":"

    Abating Risk of AD Dementia seems to appear out of nowhere. \u00a0People feel like helpless victims of their genes. \u00a0But this is a misconception. \u00a0How much does the dreaded ApoE4 gene increase your chance of getting dementia? \u00a0This is not a straightforward calculation precisely because the correlation must be controlled for many diet and lifestyle … Read more<\/a><\/p>\n","protected":false},"author":65,"featured_media":588,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"jetpack_post_was_ever_published":false,"_jetpack_newsletter_access":"","_jetpack_dont_email_post_to_subs":false,"_jetpack_newsletter_tier_id":0,"_jetpack_memberships_contains_paywalled_content":false,"_jetpack_memberships_contains_paid_content":false,"footnotes":""},"categories":[1],"tags":[],"class_list":["post-587","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-uncategorized"],"yoast_head":"\nPreventing Dementia - Josh Mitteldorf<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/scienceblog.com\/joshmitteldorf\/2017\/06\/19\/preventing-dementia\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Preventing Dementia\" \/>\n<meta property=\"og:description\" content=\"Abating Risk of AD Dementia seems to appear out of nowhere. \u00a0People feel like helpless victims of their genes. \u00a0But this is a misconception. \u00a0How much does the dreaded ApoE4 gene increase your chance of getting dementia? \u00a0This is not a straightforward calculation precisely because the correlation must be controlled for many diet and lifestyle ... 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The surprising fact that our bodies are genetically programmed to age and to die offers an enormous opportunity for medical intervention. It may be that therapies to slow the progress of aging need not repair or regenerate anything, but only need to interfere with an existing program of self-destruction. Mitteldorf has taught a weekly yoga class for thirty years. He is an advocate for vigorous self care, including exercise, meditation and caloric restriction. After earning a PhD in astrophysicist, Mitteldorf moved to evolutionary biology as a primary field in 1996. He has taught at Harvard, Berkeley, Bryn Mawr, LaSalle and Temple University. He is presently affiliated with MIT as a visiting scholar. In private life, Mitteldorf is an advocate for election integrity as well as public health. He is an avid amateur musician, playing piano in chamber groups, French horn in community orchestras. His two daughters are among the first children adopted from China in the mid-1980s. Much to the surprise of evolutionary biologists, genetic experiments indicate that aging has been selected as an adaptation for its own sake. This poses a conundrum: the impact of aging on individual fitness is wholly negative, so aging must be regarded as a kind of evolutionary altruism. Unlike other forms of evolutionary altruism, aging offers benefits to the community that are weak, and not well focussed on near kin of the altruist. This makes the mechanism challenging to understand and to model. more at http:\\\/\\\/mathforum.org\\\/~josh\",\"sameAs\":[\"http:\\\/\\\/AgingAdvice.org\"],\"url\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/author\\\/joshmitteldorf\\\/\"}]}<\/script>\n<!-- \/ Yoast SEO Premium plugin. -->","yoast_head_json":{"title":"Preventing Dementia - Josh Mitteldorf","robots":{"index":"index","follow":"follow","max-snippet":"max-snippet:-1","max-image-preview":"max-image-preview:large","max-video-preview":"max-video-preview:-1"},"canonical":"https:\/\/scienceblog.com\/joshmitteldorf\/2017\/06\/19\/preventing-dementia\/","og_locale":"en_US","og_type":"article","og_title":"Preventing Dementia","og_description":"Abating Risk of AD Dementia seems to appear out of nowhere. \u00a0People feel like helpless victims of their genes. \u00a0But this is a misconception. \u00a0How much does the dreaded ApoE4 gene increase your chance of getting dementia? \u00a0This is not a straightforward calculation precisely because the correlation must be controlled for many diet and lifestyle ... 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The surprising fact that our bodies are genetically programmed to age and to die offers an enormous opportunity for medical intervention. It may be that therapies to slow the progress of aging need not repair or regenerate anything, but only need to interfere with an existing program of self-destruction. Mitteldorf has taught a weekly yoga class for thirty years. He is an advocate for vigorous self care, including exercise, meditation and caloric restriction. After earning a PhD in astrophysicist, Mitteldorf moved to evolutionary biology as a primary field in 1996. He has taught at Harvard, Berkeley, Bryn Mawr, LaSalle and Temple University. He is presently affiliated with MIT as a visiting scholar. In private life, Mitteldorf is an advocate for election integrity as well as public health. He is an avid amateur musician, playing piano in chamber groups, French horn in community orchestras. His two daughters are among the first children adopted from China in the mid-1980s. Much to the surprise of evolutionary biologists, genetic experiments indicate that aging has been selected as an adaptation for its own sake. This poses a conundrum: the impact of aging on individual fitness is wholly negative, so aging must be regarded as a kind of evolutionary altruism. Unlike other forms of evolutionary altruism, aging offers benefits to the community that are weak, and not well focussed on near kin of the altruist. 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