SUBJ: New Mito-C tablets are available.
SUBtitle: Listening to or playing music has tremendous healthspan benefits
Links for new readers: 1) One Day in Roc’s Life: 46 resolutions to prolong health span 2) Recent important nutrition news. 3) A contribution to this newsletter is healthier and less expensive than your multivitamin. Donation link:Nutrition Newsletter.
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SHORT NOTES:
New Mito-C tablets are available.
Listening to or playing music enhances a sense of well-being, reduces stress, facilitates interpersonal connections, modulates the cardiovascular system, improves balance and boosts the immune system.
The #1 Exercise to Do as You Get Older: squats.
Omega-3 polyunsaturated fatty acids (n-3 PUFAs) can inhibit the production of interleukin 11 which is likely to extend healthspan.
mTOR inhibition extends lifespan. A 5 g dose of branched chain amino acids taken by athletes activates the mTOR pathway, decreasing lifespan.
22% of kids under 5 are malnourished to the point of stunting, costing at least 15 IQ. Malnutrition could end for $12 billion per year, “1/3rd of what America wastes on farm subsidies.”
Broccoli sprouts contain 10-100 times more glucoraphanin than a mature plant to maximize the health benefits of sulforaphane.
Only one molecule deserves vitamin E requirement: alpha-tocopherol.
Researchers have found that men and women have significant differences in how their brains’ blood vessels change in Alzheimer’s disease.
Personal digital tools can help support and motivate individuals to follow a personal diet. The precision diet group reported improvements in vitality, body pain, and emotions.
The molecule linking exercise to the inhibition of cellular senescence is pigment epithelium-derived factor.
By making NK cells insensitive to tumor-secreted TGF-β, scientists have improved their efficacy against this deadly hepatocellular carcinoma.
FeelBetter medicine interaction algorithm could reduce hospitalizations by 24%.
LONG NOTES:
New Mito-C tablets are available. See newsletter sent yesterday. Order here. You can read my web page about it here. Order here. Disclaimer: I do get $1/bottle sold for designing this supplement. It costs $34.95 per month. How much is a healthy brain worth to you?
AARP: The Global Council on Brain Health has a report, “Music on our minds” that shows music enhances a sense of well-being, reduces stress, facilitates interpersonal connections, modulates the cardiovascular system, improves balance and boosts the immune system. A study of 3,185 Americans found those who listen to or make music report better overall, brain, and cognitive health.
AARP: The #1 Exercise to Do as You Get Older: squats — the classic move in which you slowly lower your bottom to seated level, then stand back up.
[fm Roc] Omega-3 polyunsaturated fatty acids (n-3 PUFAs) can inhibit the production of interleukin 11 (IL-11) in hepatocytes (ref NIH) which is likely to extend healthspan. [GRG] The recently published study below shows extension of lifespan with IL-11 inhibition in mice. I haven’t read the full text of the study in any detail, but glancing over it this looks like a very important finding. IL-11 inhibition appears to have not only increased maximum lifespan but the median lifespan even exceeded the maximum lifespan of wild type mice in some of the experiments, which is quite remarkable. I can’t say IL-11 is something I have researched in any detail, so I don’t have much to say about this at this point.
Science 7/12 pg 156 mTOR inhibition extends lifespan. mTOR causes inflammation. When metformin treatment (Met) is added to the mTOR inhibitor rapamycin (Rap), median and maximal life span is extended. Branched chain amino acids like leucine often taken by athletes. A 5 g dose is taken by athletes after a hard workout to repair muscles. But taking a 5 g dose activates the mTOR pathway. Activating the mTOR pathway may decrease lifespan.
The Economist 7/15, pg 9-How to raise the world’s IQ-22% of kids under 5 are malnourished to the point of stunting, costing at least 15 IQ points each. Vaccinations and teaching parents about nutrition could relieve this. Malnutrition could end for $12 billion per year, “1/3rd of what America wastes on farm subsidies.”
From LPI Newsletter: Glucoraphanin found in broccoli, cauliflower, kale, cabbage, mustard greens, and Brussels sprouts can be converted to sulforaphane through a reaction catalyzed by an enzyme called myrosinase, which is also found in these vegetables. When these plants are crushed, chopped, or chewed, the enzyme reacts with glucoraphanin to produce sulforaphane (for more details, see “Broccoli FAQ” in the March-May 2022 LPI Research Newsletter). Broccoli is a good source of glucoraphanin. Broccoli sprouts (three to four-day-old broccoli plants) are an excellent source of glucoraphanin. By weight, broccoli sprouts contain 10-100 times more glucoraphanin than a mature plant, making them a convenient way to maximize the health benefits of sulforaphane.
From Maret Traber of LPI: Together, the tocopherols and tocotrienols are correctly classified as “tocochromanols” but are more commonly referred to as “eight forms of vitamin E.” As Dr. Maret Traber discussed in a recently published review in the journal Free Radical Biology and Medicine, only one molecule deserves vitamin status: alpha-tocopherol, the specific molecule that prevented the death of developing embryos. Traber outlined the consequences of vitamin E deficiency in humans, which typically manifests as neurological abnormalities in people with prolonged, severe dietary deficiencies. Only alpha-tocopherol can reverse or prevent the progression of these issues and restore health. This is not to say that the other tocopherols and tocotrienols do not have biological activity. Like many phytochemicals, tocochromanols have a role to play in promoting health, but further research is needed to properly define their purpose.
Researchers have found that men and women have significant differences in how their brains’ blood vessels change in Alzheimer’s disease. This research begins with a discussion of Alzheimer’s and its two principal symptoms: the well-known plaques that coat the brain, and the tau proteins that aggregate in neurons. However, targeting either of these proteins after they have already been formed has not been effective in preventing neurons from dying or stopping cognitive decline [1]. These researchers hypothesize that such interventions simply occur too late. Therefore, they chose to focus on something that occurs much earlier in the process: the decline of the blood-brain barrier (BBB) [2]. One consequence of the hypoxic response is angiogenesis: the creation of new blood vessels. Genes related to the hypoxic response leading to angiogenesis were strongly upregulated in men with Alzheimer’s, but in women, they were not. However, in women, a different gene, PIK3C2A, was upregulated that leads to angiogenesis; the researchers suggest that this may be a druggable target for men, who do not normally upregulate it. Estrogen also affects CREB1, and these researchers pinpointed the menopause-related decline in estrogen as being key to the onset of Alzheimer’s in women. An estrogen receptor and a receptor for a hypoxia-inducible factor both have many of the same downstream targets, and menopause is a significant risk factor for vascular disease [9]. Therefore, these researchers believe that men retain a key protection in the blood-brain barrier that post-menopausal women do not. Hormone replacement therapy for older women, therefore, may be found to be necessary to prevent late-life Alzheimer’s, or another method of activating the relevant angiogenesis pathways may be found.
Proper diets can help people stay healthy even into old age. However, nutrition advice is designed for the average person, and it does not consider the high variability among people’s nutritional needs and preferences. Personalized nutrition approaches address this need to optimize the diet for the individual. Such personalized nutrition can also be considered a therapeutic approach to preventing or managing chronic diseases.
However, sticking to a strict, individualized diet might be difficult for most people. The current study’s authors believe that digital tools can help support and motivate individuals to follow the recommended diet. Therefore, they created a trial that determined whether individualized dietary interventions alongside a digital tool can affect the health of overweight and obese older adults. Usual-care vs. individualized diet. The study included 127 participants who were between the ages of 50 and 80 and had a BMI o at least 27. Participants had to have at least one risk factor, such as type 2 diabetes, hypertension, high cholesterol, or sedentary behavior. The trial lasted 12 weeks and had a 3-month follow-up. The precision diet group received guidelines to follow a Mediterranean and mixed diet that included foods based around personal preferences, such as smoothies, fruit compote, and wholemeal bread. These foods were designed specifically for this study, and their ingredients were chosen to prevent age-related diseases. Also, only the members of this group had their caloric intake needs assessed and attended visits to supervise diet adherence. The precision diet group’s app was also specifically designed for this study with the needs of the elderly in mind, being easily accessible and easy to use. It contained information about the assigned diet, reminders about follow-up visits, and motivational messages. At the end of the study, participants filled out a dietary intake questionnaire recalling their 7-day food intake, physical activity, and health status and took tests to assess cognitive functions. Analysis of the obtained data revealed that, after three months of diet, both groups experienced significant reductions in body weight, BMI, and diastolic blood pressure. Still, the changes in the precision diet group were significantly greater than those in the usual-care group. The precision diet group also had significantly lower total cholesterol and HDL-c levels and had improved glycemic control and hepatic health markers, compared to both baseline and the usual-care group. The researchers measured total energy intake but didn’t observe differences between the groups. However, the groups differed regarding specific food groups, with carbohydrates, proteins, and fiber content significantly higher and lipids lower in the precision group. Based on the questionnaires that the participants filled out upon completion of a 3-month study, the members of the precision diet group improved their quality of life. Specifically, the precision diet group reported improvements in the quality of life test’s vitality, body pain, and emotional role section.
Researchers publishing in Aging have found a molecule linking exercise to the inhibition of cellular senescence, one of the hallmarks of aging. Exercise, among its many benefits, has been found to fight against COPD [3] and reduce cellular senescence [4]; however, previous work has not discovered the molecular underpinnings of why. These researchers searched for a connection, looking for the exercise-related factor that impedes senescence. Narrowing it down to proteins that had been previously found both to inhibit senescence and to be related to exercise, the researchers found only one that satisfies both criteria: pigment epithelium-derived factor (PEDF) [5, 6]. As you age, increasing numbers of your cells enter into a state known as senescence. These cells do not divide or support the tissues of which they are part; instead, they emit a range of potentially harmful chemical signals that encourage nearby healthy cells to enter the same senescent state. Their presence causes many problems: they reduce tissue repair, increase chronic inflammation, and can even eventually raise the risk of cancer and other age-related diseases. Worn out or badly damaged cells normally destroy themselves via a programmed cell death called apoptosis, and they are also removed by the immune system; however, the immune system weakens with age, and increasing numbers of old and damaged cells escape this process and begin to accumulate in all the tissues of the body. By the time people reach old age, significant numbers of these death resistant cells have built up, causing chronic inflammation and damage to surrounding cells and tissue. These senescent cells are a key process in the progression of aging [1-2]. Follow-up studies showed that removing just thirty percent of the cells was enough to slow down age-related decline and ill health in mice [8-10].
By making NK cells insensitive to tumor-secreted TGF-β, scientists have improved their efficacy against this deadly hepatocellular carcinoma (HCC) [1]. Cancer cells, which are supposed to be vulnerable to the immune system, develop various defensive mechanisms to avoid detection and decrease immune cells’ fitness and viability. In solid tumors, the dense tumor microenvironment (TME) has a particularly strong dampening effect on immune activity. In this new study, scientists from the University of California – San Diego combined several cutting-edge techniques to try and overcome this problem. To begin with, they used cellular reprogramming to manufacture brand-new NK cells. This involves producing induced pluripotent stem cells (iPSCs) from differentiated cells and their further re-differentiating them into NK cells. NK cells with TGFB2R knocked out and without CAR expression killed HCC cells better than CAR-expressing wild type NK cells. There was some synergy between CARs and TGFB2R knockout, albeit not a strong one. Importantly, when stressed with TGF-β, only TGFB2R-k
Preventing clash of medications. A study by Israel’s FeelBetter (see here previously) at Boston’s Mass General Brigham, of its medicine interaction algorithm shows it could reduce hospitalizations by 24%. It has now signed with New Jersey’s Atlantic Health System, which administers to over half a million Americans.
