{"id":594,"date":"2017-07-25T13:19:11","date_gmt":"2017-07-25T13:19:11","guid":{"rendered":"http:\/\/joshmitteldorf.peachpuff-wolverine-566518.hostingersite.com\/?p=594"},"modified":"2017-07-25T13:19:11","modified_gmt":"2017-07-25T13:19:11","slug":"mitochondria-in-aging-ii-remedies","status":"publish","type":"post","link":"https:\/\/scienceblog.com\/joshmitteldorf\/2017\/07\/25\/mitochondria-in-aging-ii-remedies\/","title":{"rendered":"Mitochondria in Aging, II: Remedies"},"content":{"rendered":"

The once-popular mitochondrial free radical theory of aging proved to be too glib. Aging isn\u2019t fundamentally about dispersed damage; rather, dispersed damage is a result when the body\u2019s defenses stand down in old age. \u00a0Nevertheless, the mitochondria do play a role in aging, largely through signaling and apoptosis. \u00a0Antioxidants targeted to mitochondria may be an exception to the rule that antioxidants don\u2019t prolong lifespan. \u00a0And other supplements and strategies that either promote production of new mitochondria or enhance their efficiency of operation show promise for modest lifespan extension.<\/span><\/i><\/p>\n

\n

Growing new mitochondria<\/b><\/p>\n

A ketogenic diet leads to generation of <\/span>new mitochondria<\/span><\/a>, as do caloric restriction and exercise. \u00a0Exercise when the body is starved for sugar (low glycogen) is the <\/span>most potent stimulator<\/span><\/a> of new mitochondrial growth. \u00a0Exercise while fasting, or continue to exercise after you \u201chit your wall\u201d.<\/span><\/p>\n

Hormones that promote mitochondrial proliferation include thyroxin, estrogens, and glucocorticoids. \u00a0Promoting new mitochondria has a tendency simultaneously to suppress apoptosis, programmed cell death [<\/span>ref<\/span><\/a>]. \u00a0At later ages, apoptosis of cells that are still functional tends to be a larger problem than the failure of cancerous cells to eliminate themselves by apoptosis. \u00a0In other words, suppressing apoptosis is (on balance) a good thing for anti-aging, but the downside is it can also increase risk of cancer.<\/span><\/p>\n

 <\/p>\n

Ubiquinone=CoQ10<\/b><\/p>\n

Coenzyme Q-10 (aka ubiquinone) is an essential part of mitochondrial chemistry, shuttling electrons along their way to the ATP molecules that mitochondria generate as their primary energy export to the cell. \u00a0It\u2019s often called an antioxidant, but that\u2019s not the primary role of CoQ10.<\/span><\/p>\n

As a supplement, it is well-established with a good reputation. \u00a0There is lots of evidence for benefits to health markers, especially athletic endurance, several aspects of heart health, and erectile dysfunction. \u00a0If you have fibromyalgia or if you are taking statins, CoQ10 is strongly indicated. \u00a0For chronic fatigue syndrome, it\u2019s definitely worth trying. \u00a0<\/span><\/p>\n

But there\u2019s no reason to expect it will increase your life expectancy. \u00a0Supplementing with ubiquinone increases the lifespan of <\/span>worms<\/span><\/a> but not mice or rats [<\/span>ref<\/span><\/a>, <\/span>ref<\/span><\/a>].<\/span><\/p>\n

Worms that cannot make unbiquinone live <\/span>10 times as long<\/span><\/a>. \u00a0Just saying…<\/span><\/p>\n

A few years ago, ubiquinol was introduced as a more bioavailable form of ubiquinone. \u00a0It\u2019s more expensive, but there is <\/span>not clear evidence<\/span><\/a> that it is more bioavailable.<\/span><\/p>\n

 <\/p>\n

PQQ<\/b><\/p>\n

P<\/span><\/i>yrroloquinoline quinone <\/span><\/i>is helpful but not necessary part of mitochondrial chemistry. \u00a0Bacteria make a lot of it; plants less; mammals only tiny quantities. \u00a0Mice completely deprived of PQQ show growth deficiency, but the amount that they need is tiny compared to the quantities in PQQ supplements. <\/span><\/p>\n

PQQ is a growth factor for bacteria, and the principal health claim for PQQ is that it can stimulate growth of new mitochondria. \u00a0The <\/span>evidence<\/span><\/a> is based on biochemistry and cell cultures. \u00a0In live mice, it has been shown that PQQ deficiency results in a mitochondria deficiency, but not that large quantities of PQQ lead to more mitochondria.<\/span><\/p>\n

Bill Faloon (<\/span>LEF<\/span><\/a>) and Joseph Cohen (<\/span>selfhacked<\/span><\/a>) are big fans of PQQ, and you can read a list of benefits <\/span>here<\/span><\/a>. \u00a0Cohen claims PQQ helps with <\/span>sleep quality<\/span><\/a> and <\/span>nerve growth<\/span><\/a>, leading to better <\/span>cognitive function<\/span><\/a>. \u00a0<\/span><\/p>\n

Small quantities of PQQ can be absorbed from many plant foods, but not animal foods. \u00a0<\/span>Much larger quantities come in supplement form. 100 g of tofu has just 2\u00b5g (micrograms). \u00a0Supplements are usually 5-20 mg, hundreds of times as much as you\u2019re likely to get from a vegetarian diet. \u00a0<\/span>Here<\/span><\/a> is a table of PQQ concentrations in foods: <\/span><\/p>\n

 <\/p>\n

SkQ and MitoQ<\/b><\/p>\n

These are two closely related molecules, originally synthesized in Russia in the 1970s, but it wasn\u2019t until the 1990s that their therapeutic value was documented by two New Zealand scientists. \u00a0One end of the molecule is CoQ10 (or a version found in plants, claimed to be even more powerful as an antioxidant). \u00a0The other end of the molecule is an electric tugboat that pulls the molecule into mitochondria. \u00a0<\/span><\/p>\n

I\u2019ve written a \u00a0<\/span>detailed report<\/span><\/a> three years ago. \u00a0At the time, I noted that the Russians claimed to extend lifespan of mice modestly with SkQ, and SkQ was found (also in Russian labs) to be a powerful rejuvenant for aging eyes. \u00a0The Russians sell <\/span>SkQ<\/span><\/a> as eye drops. \u00a0The Kiwis sell <\/span>MitoQ<\/span><\/a> as skin cream and also as pills. <\/span><\/p>\n

Earlier this year, the Russian labs <\/span>announced<\/span><\/a> that SkQ had substantially extended lifespan of a mouse strain that was short-lived because of a mitochondrial defect. \u00a0None of the Russian claims have been reproduced in Western labs. \u00a0Three years ago, I was inclined to give the Russians the benefit of the doubt, but now I\u2019m starting to wonder, since the New Zealand company has a laboratory arm, and they haven\u2019t announced anything nearly so impressive.<\/span><\/p>\n

 <\/p>\n

Humanin and her sisters<\/b><\/p>\n

Mitochondria have ringlets of their own DNA, encoding just 37 genes. \u00a0(That doesn\u2019t mean that the mitochondria only need 37 proteins; the great majority of proteins needed by mitochondria are coded in chromosomes of the cell nucleus, and transported to the mitochondria as needed.) \u00a0Just 16 years ago, the first mitochondrial-coded protein to be discovered was named Humanin, because it was found to improve cognitive function to dementia patients, restoring some of their \u201chumanity\u201d. \u00a0In addition to being neuroprotective, humanin promotes <\/span>insulin sensitivity<\/span><\/a>. \u00a0Humannin\u2019s action is not confined to the mitochondrion in which it was produced, but in fact it \u00a0circulates in the blood as a signal molecule. \u00a0Blood levels of humanin decline with age.<\/span><\/p>\n

Humanin<\/figcaption><\/figure>\n

In experiments with mice, humanin injections have been shown to protect against disease. \u00a0Lifespan assays with humanin are not yet available. <\/span><\/p>\n

To date, HN and its analogs have been demonstrated to play a role in multiple diseases including type 2 diabetes (<\/span>25<\/span><\/a>, <\/span>43<\/span><\/a>), cardiovascular disease (CVD) (<\/span>2<\/span><\/a>, <\/span>3<\/span><\/a>, <\/span>47<\/span><\/a>), memory loss (<\/span>48<\/span><\/a>), amyotrophic lateral sclerosis (ALS) (<\/span>49<\/span><\/a>), stroke (<\/span>50<\/span><\/a>), and inflammation (<\/span>22<\/span><\/a>, <\/span>51<\/span><\/a>). The mechanisms that are common to many of these age-related diseases are oxidative stress (<\/span>52<\/span><\/a>) and mitochondrial dysfunction (<\/span>53<\/span><\/a>). Mitochondria are major source of ROS, excess of which can cause oxidative damage of cellular lipids, proteins, and DNA. The accumulation of oxidative damage will result in decline of mitochondrial function, which in turn leads to enhanced ROS production (<\/span>53<\/span><\/a>). This vicious cycle can play a role in cellular damage, apoptosis, and cellular senescence \u2013 contributing to aging and age-related diseases. Indeed, oxidative stress is tightly linked to multiple human diseases such as Parkinson\u2019s disease (PD) (<\/span>54<\/span><\/a>), AD (<\/span>55<\/span><\/a>), atherosclerosis (<\/span>56<\/span><\/a>), heart failure (<\/span>57<\/span><\/a>), myocardial infarction (<\/span>58<\/span><\/a>), chronic inflammation (<\/span>59<\/span><\/a>), kidney disease (<\/span>60<\/span><\/a>), stroke (<\/span>61<\/span><\/a>), cancers (<\/span>62<\/span><\/a>, <\/span>63<\/span><\/a>), and many types of metabolic disorders (<\/span>64<\/span><\/a>, <\/span>65<\/span><\/a>). We and others have shown that HN plays critical roles in reducing oxidative stress (<\/span>66<\/span><\/a>\u2013<\/span>68<\/span><\/a>). [<\/span>2014 review<\/span><\/a>]<\/span><\/p>\n

Pinchas Cohen, MD (Dean, School of Gerontology, University of Southern California Davis, Los Angeles, California) is an expert in humanin, a protein (peptide) produced in mitochondria. Mitochondria are energy-generating organelles in cells, which have their own DNA separate from the DNA in the nucleus.<\/span> The amount of DNA found in the mitochondria is much less than that found in the nucleus. As such, mitochondrial DNA contains codes for only a few proteins, humanin being one of them. Humanin was discovered by a search for factors helping to keep neurons alive in undiseased portions of the brains of Alzheimer\u2019s disease patients.<\/span> Humanin protects neurons against cell death in Alzheimer\u2019s disease, as well as protecting against toxic chemicals and prions (toxic proteins)[<\/span>ref<\/span><\/a>]. <\/span>\u00a0<\/span>Dr. Cohen\u2019s team has shown that humanin also protects cells lining blood vessel walls, preventing atherosclerosis. In particular, they have shown that low levels of humanin in the bloodstream are associated with endothelial dysfunction of the coronary arteries (arteries of the heart).[<\/span>ref<\/span><\/a>] Humanin has also been shown to promote insulin sensitivity, the responsiveness of tissues to insulin.<\/span> Because humanin levels decline with age, it is believed that reduced humanin contributes to the development of aging-associated diseases, including Alzheimer\u2019s disease and type II diabetes.<\/span> [<\/span>Ben Best<\/span><\/a>]<\/span><\/em><\/p><\/blockquote>\n

Personal notes: This <\/span>lab near where I am visiting in Beijing<\/span><\/a> is taking leadership in characterizing a group of short peptides similar in origin to humanin, and this <\/span>company across the street from us<\/span><\/a> is selling mitochondrial peptides.<\/span><\/p>\n

If humanin were a patentable drug, there would be much excitement and multiple clinical trials for AD, probably leading to expansion into general anti-aging effects.<\/span><\/p>\n

 <\/p>\n

MOTS-c<\/b><\/p>\n

This is another short peptide of mitochondrial origin, only recently discovered and characterized. \u00a0I was alerted to its existence by a study from a <\/span>USC lab<\/span><\/a> that was written up <\/span>here in ScienceBlog<\/span><\/a> just this month (reprinted from a <\/span>USC press release<\/span><\/a>). \u00a0Results are new but impressive. \u00a0Mice injected with MOTS-c had more muscle mass, less fat, more strength and endurance. \u00a0MOTS-c protected their insulin sensitivity when mice were fed a high fat diet [<\/span>ref<\/span><\/a>]. \u00a0Lifespan studies haven\u2019t been done yet.<\/span><\/p>\n

Like humanin, MOTS-c is manufactured inside mitochondria from a template in mitochondrial DNA, but it is exported from the cell and appears in the bloodstream as a signal molecule. \u00a0Blood levels of MOTS-c decline with age. \u00a0It is a mini protein molecule with 16 amino acids, too big to survive digestion so it can\u2019t be taken orally. \u00a0<\/span><\/p>\n

\u201c<\/span>MOTS-c holds much potential as a target to treat metabolic syndromes by regulating muscle and fat physiology, and perhaps even extend our healthy lifespan.<\/span>\u201d[<\/span>ref<\/span><\/a>]<\/span><\/p>\n

Let\u2019s keep your eyes on this one over the next year or two.<\/span><\/p>\n

 <\/p>\n

Gutathione \/ NAC<\/b><\/p>\n

I\u2019ve never heard anyone say a bad word about glutathione. \u00a0It\u2019s the antioxidant with no downside. \u00a0Genetic modifications that upregulate glutathione have increased lifespan in worms, flies and mice. \u00a0<\/span><\/p>\n

For a long while, it has been assumed that you can\u2019t eat glutathione, because it doesn\u2019t survive digestion. \u00a0Some researchers at Penn State disagree<\/a>, finding impressive increases in tissue and blood levels when people were supplemented with up to 1 g per day raw glutathione. \u00a0Liposomal glutathione<\/a> is an oral delivery form that gets around the digestion problem, especially when taken with methyl donors like SAMe.<\/p>\n

The herb Sylimarin=milk thistle may increase glutathione<\/a>. \u00a0For now, the precursor molecule N-Acetyl Cysteine (NAC) is the best-established supplement we have to promote glutathione. \u00a0In the one available study<\/a>, supplementing with NAC greatly increased lifespan in male but not female mice. \u00a0NAC also increases lifespan in worms<\/a> and flies<\/a>.<\/p>\n

N-Acetyl Cysteine<\/figcaption><\/figure>\n
\"\"
Glutathione<\/figcaption><\/figure>\n

 <\/p>\n

For the future, we might hope to do better. \u00a0Less than 20% of the cell\u2019s glutathione actually makes its way to the mitochondria, where it is most needed. \u00a0There are esters of glutathione that, in theory, ought to be attracted into the mitochondria. \u00a0They have been tested in cell culture only, but are more than ripe for animal testing [ref<\/a>].<\/p>\n

 <\/p>\n

Nicotinamide Riboside (NR) and other NAD+ enhancers<\/b><\/p>\n

The chemicals NAD+ and NADH are alternative, cycled forms of an intermediate in the process by which mitochondria make energy. \u00a0Levels of NAD+\/NADH decline with age. \u00a0NR is a precursor to NAD+, and it has been demonstrated (preliminary results in humans<\/a>) that NR supplementation increases blood levels of NAD+.<\/p>\n

It may be awhile before we know for sure whether this leads to better health or longer lifespan. \u00a0Niagen and Basis are heavily promoted with credible scientifists behind their products, and many early adopters offer subjective reports<\/a> of short-term benefits. \u00a0There is one mouse study<\/a> claiming to pull a 3% extension of lifespan out of the noise, and perhaps I am less open to the finding because the article, published prominently in Science, seems so breathless in describing benefits.<\/p>\n

 <\/p>\n

Melatonin<\/b><\/p>\n

The primary role of melatonin is to regulate the body\u2019s sleep\/wake cycle. \u00a0Melatonin declines with age and the timing of our daily melatonin surge gets fuzzier and less reliable with age.sleep quality deteriorates. \u00a0Sleep quality suffers.<\/p>\n

Melatonin is well-established in mice as a modest longevity aid, although results have been inconsistent<\/a>. \u00a012 out of 20 studies showed a lifespan increase, and the remaining 8 showed no increase or decrease. \u00a0Whether nightly supplementation affects mortality rates in humans has never been determined.<\/p>\n

Melatonin is concentrated in mitochondria as much as 100-fold, and it may even be created there [ref<\/a>], independent of the circulating melatonin that is secreted from the pineal gland at night. \u00a0One of its actions is as a mitochondrial antioxidant and scavenger of ROS.<\/p>\n

Twenty years ago, Walter Pierpaoli<\/a> promoted melatonin as a sleep aid, cancer fighting hormone that would enhance your mood and your sex life while keeping you young. \u00a0Russian labs have also been optimistic. \u00a0My take is that melatonin is a legitimate anti-aging hormone, and is especially useful for those of us whose sleep is disrupted with age. \u00a0It is widely available, cheap and safe. \u00a0Unless you’re fighting jet lag, 1 to 2 mg at night is all you need.<\/p>\n

Also worth mentioning<\/strong><\/p>\n

Magnesium is required for manufacture of glutathione. \u00a0Selenium works along with glutathione. \u00a0Omega-3 fatty acids can promote synthesis of glutathione.\u00a0\u00a0Acetyl L-carnitine transports fat fuels through the mitochondrial membrane. \u00a0Alpha-lipoic acid is part of the mitochondrial energy metabolism.<\/p>\n

The Bottom Line<\/b><\/p>\n

Commercial interests can make some messages louder than others, and the health news we hear is affected by what is profitable as much as by what is healthy. \u00a0Exercise is primary, but has no sales value. \u00a0Of the supplements reviewed here, NAC is the best-established for mitochondrial health and a possible effect on lifespan. \u00a0It is cheap and available. \u00a0Liposomal glutathione is certainly more expensive and possibly more effective. \u00a0Melatonin is even cheaper, and has been found to increase lifespan in multiple rodent studies, with broad benefits apart from modification of mitochondrial function. \u00a0Humanin and MOTS-c, not yet close to commercial availability, seem to be promising substances to explore for health, though not for profits.<\/p>\n","protected":false},"excerpt":{"rendered":"

The once-popular mitochondrial free radical theory of aging proved to be too glib. Aging isn\u2019t fundamentally about dispersed damage; rather, dispersed damage is a result when the body\u2019s defenses stand down in old age. \u00a0Nevertheless, the mitochondria do play a role in aging, largely through signaling and apoptosis. \u00a0Antioxidants targeted to mitochondria may be an … Read more<\/a><\/p>\n","protected":false},"author":65,"featured_media":596,"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-594","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-uncategorized"],"yoast_head":"\nMitochondria in Aging, II: Remedies - 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\/07\/25\/mitochondria-in-aging-ii-remedies\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Mitochondria in Aging, II: Remedies\" \/>\n<meta property=\"og:description\" content=\"The once-popular mitochondrial free radical theory of aging proved to be too glib. Aging isn\u2019t fundamentally about dispersed damage; rather, dispersed damage is a result when the body\u2019s defenses stand down in old age. \u00a0Nevertheless, the mitochondria do play a role in aging, largely through signaling and apoptosis. \u00a0Antioxidants targeted to mitochondria may be an ... 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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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