Category Archives: Aging

Aging and NAD

A conserved NAD+ binding pocket interactions during aging


Story from Sciencedaily copied and pasted:

DNA repair is essential for cell vitality, cell survival and cancer prevention, yet cells’ ability to patch up damaged DNA declines with age for reasons not fully understood.

Now, research led by scientists at Harvard Medical School reveals a critical step in a molecular chain of events that allows cells to mend their broken DNA.

The findings, published March 24 in Science, offer a critical insight into how and why the body’s ability to fix DNA dwindles over time and point to a previously unknown role for the signaling molecule NAD as a key regulator of protein-to-protein interactions in DNA repair. NAD, identified a century ago, is already known for its role as a controller of cell-damaging oxidation.

Additionally, experiments conducted in mice show that treatment with the NAD precursor NMN mitigates age-related DNA damage and wards off DNA damage from radiation exposure.

The scientists caution that the effects of many therapeutic substances are often profoundly different in mice and humans owing to critical differences in biology. However, if affirmed in further animal studies and in humans, the findings can help pave the way to therapies that prevent DNA damage associated with aging and with cancer treatments that involve radiation exposure and some types of chemotherapy, which along with killing tumors can cause considerable DNA damage in healthy cells. Human trials with NMN are expected to begin within six months, the researchers said.

“Our results unveil a key mechanism in cellular degeneration and aging but beyond that they point to a therapeutic avenue to halt and reverse age-related and radiation-induced DNA damage,” said senior author David Sinclair, professor in the Department of Genetics at HMS and professor at the University of New South Wales School of Medicine in Sydney, Australia.

A previous study led by Sinclair showed that NMN reversed muscle aging in mice.

A plot with many characters

The investigators started by looking at a cast of proteins and molecules suspected to play a part in the cellular aging process. Some of them were well-known characters, others more enigmatic figures.

The researchers already knew that NAD, which declines steadily with age, boosts the activity of the SIRT1 protein, which delays aging and extends life in yeast, flies and mice. Both SIRT1 and PARP1, a protein known to control DNA repair, consume NAD in their work.

Another protein DBC1, one of the most abundant proteins in humans and found across life forms from bacteria to plants and animals, was a far murkier presence. Because DBC1 was previously shown to inhibit vitality-boosting SIRT1, the researchers suspected DBC1 may also somehow interact with PARP1, given the similar roles PARP1 and SIRT1 play.

“We thought if there is a connection between SIRT1 and DBC1, on one hand, and between SIRT1 and PARP1 on the other, then maybe PARP1 and DBC1 were also engaged in some sort of intracellular game,” said Jun Li, first author on the study and a research fellow in the Department of Genetics at HMS.

They were.

To get a better sense of the chemical relationship among the three proteins, the scientists measured the molecular markers of protein-to-protein interaction inside human kidney cells. DBC1 and PARP1 bound powerfully to each other. However, when NAD levels increased, that bond was disrupted. The more NAD present inside cells, the fewer molecular bonds PARP1 and DBC1 could form. When researchers inhibited NAD, the number of PARP1-DBC1 bonds went up. In other words, when NAD is plentiful, it prevents DBC1 from binding to PARP1 and meddling with its ability to mend damaged DNA.

What this suggests, the researchers said, is that as NAD declines with age, fewer and fewer NAD molecules are around to stop the harmful interaction between DBC1 and PARP1. The result: DNA breaks go unrepaired and, as these breaks accumulate over time, precipitate cell damage, cell mutations, cell death and loss of organ function.

Averting mischief

Next, to understand how exactly NAD prevents DBC1 from binding to PARP1, the team homed in on a region of DBC1 known as NHD, a pocket-like structure found in some 80,000 proteins across life forms and species whose function has eluded scientists. The team’s experiments showed that NHD is an NAD binding site and that in DBC1, NAD blocks this specific region to prevent DBC1 from locking in with PARP1 and interfering with DNA repair.

And, Sinclair added, since NHD is so common across species, the finding suggests that by binding to it, NAD may play a similar role averting harmful protein interactions across many species to control DNA repair and other cell survival processes.

To determine how the proteins interacted beyond the lab dish and in living organisms, the researchers treated young and old mice with the NAD precursor NMN, which makes up half of an NAD molecule. NAD is too large to cross the cell membrane, but NMN can easily slip across it. Once inside the cell, NMN binds to another NMN molecule to form NAD.

As expected, old mice had lower levels of NAD in their livers, lower levels of PARP1 and a greater number of PARP1 with DBC1 stuck to their backs.

However, after receiving NMN with their drinking water for a week, old mice showed marked differences both in NAD levels and PARP1 activity. NAD levels in the livers of old mice shot up to levels similar to those seen in younger mice. The cells of mice treated with NMN also showed increased PARP1 activity and fewer PARP1 and DBC1 molecules binding together. The animals also showed a decline in molecular markers that signal DNA damage.

In a final step, scientists exposed mice to DNA-damaging radiation. Cells of animals pre-treated with NMN showed lower levels of DNA damage. Such mice also didn’t exhibit the typical radiation-induced aberrations in blood counts, such as altered white cell counts and changes in lymphocyte and hemoglobin levels. The protective effect was seen even in mice treated with NMN after radiation exposure.

Taken together, the results shed light on the mechanism behind cellular demise induced by DNA damage. They also suggest that restoring NAD levels by NMN treatment should be explored further as a possible therapy to avert the unwanted side effects of environmental radiation, as well as radiation exposure from cancer treatments.

In December 2016, a collaborative project between the Sinclair Lab and Liberty Biosecurity became a national winner in NASA’s iTech competition for their concept of using NAD-boosting molecules as a potential treatment in cosmic radiation exposure during space missions.

Co-authors on the research included Michael Bonkowski, Basil Hubbard, Alvin Ling, Luis Rajman, Sebastian Moniot, Clemens Steegborn, Dapeng Zhang, L. Aravind, Bo Qin, Zhenkun Lou, and Vera Gorbunova.

The work was funded by the Glenn Foundation for Medical Research, the American Federation for Aging Research, Edward Schulak, grants from the National Institute on Aging and the National Institutes of Health, by the National Library of Medicine/NIH intramural program, the National Cancer Institute, and by Deutsche Forschungsgemeinschaft.

Aging increases cell-to-cell transcriptional variability upon immune stimulation

Scientists have resolved a key question in aging research by showing how mouse immune cells of different ages respond to stimulation. Study demonstrates weaker response of older cells is due to their coordination breaking down, making their response to immune stimulation more variable. Single-cell sequencing technology allows scientists to profile individual cells independently to view cellular activity in high resolution.

Aging is characterized by progressive loss of physiological and cellular functions, but the molecular basis of this decline remains unclear. We explored how aging affects transcriptional dynamics using single-cell RNA sequencing of unstimulated and stimulated naïve and effector memory CD4+ T cells from young and old mice from two divergent species. In young animals, immunological activation drives a conserved transcriptomic switch, resulting in tightly controlled gene expression characterized by a strong upregulation of a core activation program, coupled with a decrease in cell-to-cell variability. Aging perturbed the activation of this core program and increased expression heterogeneity across populations of cells in both species. These discoveries suggest that increased cell-to-cell transcriptional variability will be a hallmark feature of aging across most, if not all, mammalian tissues.

Metabolic Damage and Premature Thymus Aging Caused by Stromal Catalase Deficiency

Scientists from the Florida campus of The Scripps Research Institute (TSRI) have shown how aging cripples the production of new immune cells, decreasing the immune system’s response to vaccines and putting the elderly at risk of infection. The study goes on to show that antioxidants in the diet slow this damaging process.

The research, published August 6 in the journal Cell Reports, focused on an organ called the thymus, which produces T lymphocytes, critical immune cells that must be continuously replenished to respond to new infections.

“The thymus begins to atrophy rapidly in very early adulthood, simultaneously losing its function,” said TSRI Professor Howard Petrie. “This new study shows for the first time a mechanism for the long-suspected connection between normal immune function and antioxidants.”

Scientists have been hampered in their efforts to develop specific immune therapies for the elderly by a lack of knowledge of the underlying mechanisms of this process.

To explore these mechanisms, Dr. Petrie and his team developed a computational approach for analyzing the activity of genes in two major thymic cell types — stromal cells and lymphoid cells — in mouse tissues, which are similar to human tissues in terms of function and age-related atrophy. The team found that stromal cells were specifically deficient in an antioxidant enzyme called catalase, which resulted in elevated levels of the reactive oxygen by-products of metabolism and, subsequently, accelerated metabolic damage.

To confirm the central role of catalase, the scientists increased levels of this enzyme in genetically altered animal models, resulting in preservation of thymus size for a much longer period. In addition, animals that were given two common dietary antioxidants, including vitamin C, were also protected from the effects of aging on the thymus.

Taken together, the findings provide support for the “free-radical theory” of aging, which proposes that reactive oxygen species such as hydrogen peroxide, produced during normal metabolism, cause cellular damage that contributes to aging and age-related diseases.

While other studies have suggested that sex hormones, particularly androgens such as testosterone, play a major role in the aging process, it fails to answer the key question — why does the thymus atrophy so much more rapidly than other body tissues?

“There’s no question that the thymus is remarkably responsive to androgens,” Dr. Petrie noted, “but our study shows that the fundamental mechanism of aging in the thymus, namely accumulated metabolic damage, is the same as in other body tissues. However, the process is accelerated in the thymus by a deficiency in the essential protective effects of catalase, which is found at higher levels in almost all other body tissues.”

Unrelated but neat:

  1. Meghan E. McGee-Lawrence Karl H. Wenger Sudipta Misra Catherine L. Davis Norman K. Pollock Mohammed Elsalanty Kehong Ding Carlos M. Isales Mark W. Hamrick Joanna R. Erion Marlena Wosiski-Kuhn Phonepasong Arounleut Mark P. Mattson Roy G. Cutler Jack C. Yu Alexis M. Stranahan. Whole-body Vibration Mimics the Metabolic Effects of Exercise in Male Leptin Receptor Deficient Mice. Endocrinology, 2017 DOI: 10.1210/en.2016-1250


    Whole-body vibration has gained attention as a potential exercise mimetic, but direct comparisons with the metabolic effects of exercise are scarce. To determine whether whole-body vibration recapitulates the metabolic and osteogenic effects of physical activity, we exposed male wildtype (Wt) and leptin receptor deficient (db/db) mice to daily treadmill exercise or whole-body vibration for three months. Body weights were analyzed and compared with Wt and db/db mice that remained sedentary. Glucose and insulin tolerance testing revealed comparable attenuation of hyperglycemia and insulin resistance in db/db mice following treadmill exercise or whole-body vibration. Both interventions reduced body weight in db/db mice and normalized muscle fiber diameter. Treadmill exercise and whole-body vibration also attenuated adipocyte hypertrophy in visceral adipose tissue and reduced hepatic lipid content in db/db mice. Although the effects of leptin receptor deficiency on cortical bone structure were not eliminated by either intervention, exercise and whole-body vibration increased circulating levels of osteocalcin in db/db mice. In the context of increased serum osteocalcin, the modest effects of TE and WBV on bone geometry, mineralization, and biomechanics may reflect subtle increases in osteoblast activity in multiple areas of the skeleton. Taken together, these observations indicate that whole-body vibration recapitulates the effects of exercise on metabolism in type 2 diabetes.

A less strenuous form of exercise known as whole-body vibration (WBV) can mimic the muscle and bone health benefits of regular exercise in mice, according to a new study. WBV consists of a person sitting, standing or lying on a machine with a vibrating platform. When the machine vibrates, it transmits energy to the body, and muscles contract and relax multiple times during each second.

A less strenuous form of exercise known as whole-body vibration (WBV) can mimic the muscle and bone health benefits of regular exercise in mice, according to a new study published in the Endocrine Society’s journal Endocrinology.

WBV consists of a person sitting, standing or lying on a machine with a vibrating platform. When the machine vibrates, it transmits energy to the body, and muscles contract and relax multiple times during each second.

Many people find it challenging to exercise regularly and that is contributing to the obesity and diabetes epidemics. These disorders can increase the risk of bone fractures. Physical activity can help to decrease this risk and reduce the negative metabolic effects of each condition.

“Our study is the first to show that whole-body vibration may be just as effective as exercise at combatting some of the negative consequences of obesity and diabetes,” said the study’s first author, Meghan E. McGee-Lawrence, Ph.D., of Augusta University in Augusta, Ga. “While WBV did not fully address the defects in bone mass of the obese mice in our study, it did increase global bone formation, suggesting longer-term treatments could hold promise for preventing bone loss as well.”

To conduct the study, researchers examined two groups of 5-week-old male mice. One group consisted of normal mice, while the other group was genetically unresponsive to the hormone leptin, which promotes feelings of fullness after eating. Mice from each group were assigned to sedentary, WBV or treadmill exercise conditions.

After a week-long period to grow used to the exercise equipment, the groups of mice began a 12-week exercise program. The mice in the WBV group underwent 20 minutes of WBV at a frequency of 32 Hz with 0.5g acceleration each day. Mice in the treadmill group walked for 45 minutes daily at a slight incline. For comparison, the third group did not exercise. Mice were weighed weekly during the study.

The genetically obese and diabetic mice showed similar metabolic benefits from both WBV and exercising on the treadmill. Obese mice gained less weight after exercise or WBV than obese mice in the sedentary group, although they remained heavier than normal mice. Exercise and WBV also enhanced muscle mass and insulin sensitivity in the genetically obese mice. Although there were no significant effects in the young healthy mice, the low-intensity exercise and WBV protocols were designed for successful completion by obese mice. These findings suggest that WBV may be a useful supplemental therapy to combat metabolic dysfunction in individuals with morbid obesity.

Parkinson’s Disease risk decreased by Nicotine intake; Eat more potatoes, tomatoes, and Peppers!

Peppers, Eggplant, tomatoes, potatoes have nicotine, which seems to decrease the risk of Parkinson's Disease.
Peppers, Eggplant, tomatoes, potatoes have nicotine, which seems to decrease the risk of Parkinson’s Disease.

Nicotine from edible Solanaceae and risk of Parkinson disease

There have been found associations of cigarette smoking with a decrease in the occurrence of Parkinson’s Disease (PD):

Parkinson’s Disease Risks Associated with Cigarette Smoking, Alcohol Consumption, and Caffeine Intake

The abstract of this study is below in which smoking and coffee intake both currently decrease the risk of PD:

A reduced risk for Parkinson’s disease (PD) among cigarette smokers has been observed consistently during the past 30 years. Recent evidence suggests that caffeine may also be protective. Findings are presented regarding associations of PD with smoking, caffeine intake, and alcohol consumption from a case-control study conducted in western Washington State in 1992–2000. Incident PD cases (n = 210) and controls (n = 347), frequency matched on gender and age were identified from enrollees of the Group Health Cooperative health maintenance organization. Exposure data were obtained by in-person questionnaires. Ever having smoked cigarettes was associated with a reduced risk of PD (odds ratio (OR) = 0.5, 95% confidence interval (CI): 0.4, 0.8). A stronger relation was found among current smokers (OR = 0.3, 95% CI: 0.1, 0.7) than among ex-smokers (OR = 0.6, 95% CI: 0.4, 0.9), and there was an inverse gradient with pack-years smoked (trend p < 0.001). No associations were detected for coffee consumption or total caffeine intake or for alcohol consumption. However, reduced risks were observed for consumption of 2 cups/day or more of tea (OR = 0.4, 95% CI: 0.2, 0.9) and two or more cola drinks/day (OR = 0.6, 95% CI: 0.3, 1.4). The associations for tea and cola drinks were not confounded by smoking or coffee consumption. Am J Epidemiol 2002;155:732–8.

But cigarette smoking is bad for your lungs, increasing cancer risks and emphysema among other things, so why would anyone want to smoke just to decrease PD risk? Is there another way to decrease PD risk and why do cigarettes work for PD?

  • The study at the top of the page (ANN NEUROL 2013;74:472–477) helps demonstrate the possibility that nicotine is neuro-protective among all the millions of compounds found in cigarette smoke.
  • Nicotine is derived from nicotiana spp. of solanaceae species which includes capsicum and solanum species whose edible fruits and tubers include peppers, eggplants, potatoes, and tomatoes. All of these have nicotine in them. In peppers, there is approximately 102 micrograms/kg, while tomatoes have 43 mcg/kg of nicotine. A potato has ~19 mcg/kg of nicotine. Since we consume more tomatoes and potatoes than peppers, they make up most of the nicotine consumption in people.
  • It is noted that nicotine stimulates alpha4beta2 (a4B2) receptors in the brain which protect dopaminergic neurons by binding the receptors. This may be how PD is prevented.
  • In the study, 490 people with PD were assessed for vegetable intake, in particular peppers, tomatoes, and potatoes. It  was found that PD frequency was inversely related to solanaceae intake but not other vegetables, in particular peppers. Weighted for those with the most nicotine intake,  those with the highest nicotine consumption had the lowest frequency of PD. There were 644 controls in this study.
  • After calculating risks, pepper consumption 2-4 times a week was associated with a 30% reduction in PD risk in people who did not smoke.
  • The food impact was highest in non-smokers since the nicotine content in food is so much lower than the intake of nicotine in active smokers.
  • There was an inverse association of PD in consumption of tomatoes (Fall PA, Fredrikson M, Axelson O, et al. Nutritional and occupational factors influencing the risk of Parkinson’s disease: a casecontrol study in southeastern Sweden. Mov Disord 1999;14:28–37) , potatoes ( Hellenbrand W, Seidler A, Boeing H, et al. Diet and Parkinson’s disease. I: A possible role for the past intake of specific foods and food groups. Results from a self-administered food-frequency questionnaire in a case-control study. (Neurology 1996;47: 636–643) and a Mediterranean Diet with tomatoes ( The Association between Mediterranean Diet Adherence and Parkinson’s Disease ) [ Abstract: The most consistent data support the association between higher consumption of dairy products and increased PD risk. More recently, a prospective analysis of two large cohorts, the Health Professionals Follow-Up Study (HPFS) and the Nurses’ Health Study (NHS), revealed an association between PD risk and dietary patterns as assessed by the Alternate Healthy Eating Index (AHEI) and the alternate Mediterranean Diet Score. The Mediterranean diet (MeDi) has received attention in recent years because of growing evidence associating MeDi with lower risk for AD, cardiovascular disease, several forms of cancer, and overall mortality.The MeDi is characterized by high intake of vegetables, legumes, fruits, and cereals; high intake of unsaturated fatty acids (mostly in the form of olive oil) compared to saturated fatty acids; a moderately high intake of fish; a low to-moderate intake of dairy products, meat and poultry; and a regular but moderate consumption of ethanol, primarily in the form of wine and generally during meals. This study suggests that lower adherence to MeDi is associated with PD status. The association persisted after adjustment for multiple potential confounders. The fact that among PD participants, lower adherence was associated with earlier PD age-at-onset further suggests a possible dose-response effect. The relation between MeDi adherence and PD status was not driven by any individual category of the diet but rather the whole pattern. Previous studies have indicated that environmental factors play a major role in PD; however, most nutritional studies in PD have shown conflicting results. Possible explanation for the conflicting data is that most studies have focused on single nutrients, e.g. vitamins C or E,7,  rather than on dietary patterns. Indeed, the largest prospective study of dietary patterns identified a Mediterranean-like diet as protective of PD both in males (HPFS) and females (NHS). Assessing dietary patterns may be more informative than assessing specific nutrients separately. First, this approach is more consistent with individuals’ eating habits, and second, it takes into account interactions among nutrients. This approach has been successful in AD and in non-neurological diseases.The mechanism by which MeDi may be protective in neurodegenerative disorders is largely unknown. Mechanisms that have been hypothesized in the AD literature, include oxidative stress and inflammation. Indeed, oxidative stress has been implicated in the pathogenesis of PD.  Complex phenols and other substances including vitamin C, vitamin E, and carotenoid may serve as antioxidants,  and are found in high concentrations in the typical components of the MeDi. Inflammation has also been implicated in the pathogenesis of PD, and anti-inflammatory non-steroidal medications may be associated with a lower risk for PD. Adherence to the MeDi may attenuate inflammation. In addition, MeDi adherence may be protective because of lower consumption of compounds which are associated with higher PD risk. We and others have shown an association between animal fat consumption and PD,  and the association between higher dairy intake and PD was previously reported.]
  • There are still unknowns in this study – i.e relative to smoking, diet is a modest contributor of nicotine. Biological effects of Solanaceae nicotine has not been established but substantial a4B2 nicotine receptors are occupied without active smoking in patients who take in solanaceae products.As compared to smoking, smokers with just a puff get enough nicotine to occupy a third of the receptors for more than three hours. It is also unknown if french fries, salsa, sauces, or fried potatoes give a similar nicotine effect as the original vegetable.
  • There may be other neuroprotective chemicals in these vegetables such as Anatabine, which is antiinflammatory and has less toxicity. Anatabine Ameliorates Experimental Autoimmune thyroiditis << Key components: Tobacco smoking has numerous detrimental effects on human health, but it has also been associated with a few apparent salutary actions, including the amelioration of autoimmune (Hashimoto) thyroiditis and ulcerative colitis. Smokers in the Third National Health and Nutrition Examination Survey were found to have lower prevalence of thyroperoxidase and/or thyroglobulin antibodies than nonsmokers (1). This protective effect of smoking was confirmed in two additional cross-sectional studies, one from the Amsterdam autoimmune thyroid disease cohort (2) and the other from the Danish population (3), as well as in a 5-yr prospective study also based on the Amsterdam autoimmune thyroid disease cohort (4). In the prospective study, cigarette smoking women who had one or more relative with documented thyroid autoimmunity but no thyroid dysfunction or autoantibodies at study entry showed lower odds of developing thyroperoxidase and/or thyroglobulin antibodies (4). Similarly in ulcerative colitis, smoking has been shown to decrease flares (5), hospitalizations (6), and a need for oral glucocorticoids (7) so that low-dose smoking resumption has been successfully used in ex-smokers with refractory disease (8). The mechanisms underlying this influence of tobacco smoking on some autoimmune diseases have been related to the effects of tobacco components on the immune system (9). There are numerous (4000) components in tobacco, including alkaloids (such as nicotine and anatabine), gases (e.g. carbon monoxide), and carcinogens (e.g. polycyclic aromatic hydrocarbons, aldehydes, free radicals, and solvents), and of them nicotine is known to possess antiinflammatory properties (10). Nicotine acts via binding to the nicotinic receptor, a pentameric ion channel (mainly for sodium and calcium) formed by the arrangement of 16 different subunits in hetero- or homomeric conformations (11). The receptor is classically expressed in the peripheral (all preganglionic fibers and neuromuscular synapses) and central nervous system, but more recently it has been described in cells of the immune system, including CD4 T lymphocytes, dendritic cells, and macrophages (12). Indeed, the 7-homopentameric nicotinic receptor has emerged as a novel therapeutic target for diseases with an inflammatory pathogenesis (13). Nicotine has been used successfully in mice with experimental autoimmune encephalomyelitis in which it reduced disease severity, shifting the autoimmune profile from pathogenic Th1 and Th17 responses to protective Th2 responses (14). Nicotine, however, cannot be used in humans because it is addictive and toxic and has a short 3-h plasma half-life. Consequently, we reasoned that other alkaloids of tobacco could share similar antiinflammatory properties but have a more favorable pharmacological profile. The minor tobacco alkaloid anatabine is nonaddictive and nontoxic at therapeutic doses and has a longer 8-hr half-life. Furthermore, anatabine has been recently shown to inhibit nuclear factor-B (NF-B) activation and reduce neuroinflammation in a mouse model of Alzheimer disease (15). In the present study, we therefore tested the antiinflammatory properties of anatabine in a mouse model of experimental autoimmune thyroiditis.  Anatabine is an alkaloid with a structure similar to nicotine, found in tobacco and other solanaceous plantsas tomatoes, potatoes, green pepper, and eggplant. Its lack of addictive potential or any demonstrated toxicity. Given the structure similarity with nicotine, we postulated that anatabine initiates its effects by binding to the nicotine receptor and modulating the cholinergic control of inflammation (10, 24). The nicotinic receptor that has been clearly associated with antiinflammatory responses is the 7-homopentamer, classically found on neural cells but also on immune cells (12). Activation of the 7-nicotinic receptor present in lymphocytes, dendritic cells, and macrophages has been shown to suppress nuclear translocation of NF-B and transcription of high mobility group box 1, ultimately decreasing danger signals that initiate inflammation (25). Consistent with this mechanism, Paris and colleagues demonstrated that anatabine suppresses in a dose-dependent manner the transcription of NF-B induced by tumor necrosis factor- (15). However, anatabine suppressed the thyroidal expression of IL-18 and IL-1R2. IL-18, a member of the IL-1 family, is produced by activated macrophages and stimulates production of interferon- from T cells and natural killer cells (26), overall acting as a proinflammatory stimulus. IL-18 has been shown to increase during thyroid inflammation both in vitro (27) and in vivo (28) ]
  • Capsinoids in peppers and capsaicinoids in spicy peppers may activat TRPV1 (Transient Receptor Potential Cation Channel subfamily vanilloid member 1) in the midbrain dopaminergic neurons. This seems to e protective. Transient Receptor Potential Vanilloid Subtype 1 Mediates Cell Death of Mesencephalic Dopaminergic Neurons In Vivo and In Vitro and Somatostatin prevents lipopolysaccharide‑induced neurodegenration
  • Major nutritional issues in the management of Parkinson’s disease

Summary: To safely decrease your risk of Parkinson’s disease, increase your peppers, tomatoes, potatoes, and eggplant intake. They have nicotine that when consumed, is protective of dopaminergic receptors of your brain and seem to decrease the risk of PD.

Diet and Parkinson’s disease I A possiblerole for intake of specific foods and food groups

Systematic review and meta-analysis of hydrocarbon exposure and the risk of Parkinson’s disease.

Metals and Neuronal Metal Binding Proteins Implicated in Alzheimer’s Disease.

Outdoor work and risk for Parkinson’s disease

Inverse associations of outdoor activity and vitamin D intake with the risk of Parkinson’s disease.

Iron and Oxidative Stress in Parkinson’s Disease An Observational Study of Injury Biomarkers

Can Tea Consumption be a Safe and Effective Therapy Against Diabetes Mellitus-Induced Neurodegeneration

Parkinson’s disease no milk today

Parkinson’s Disease Risks Associated with Cigarette Smoking, Alcohol Consumption, and Caffeine Intake n

Ferritin levels in the cerebrospinal fluid predict Alzheimer’s disease outcomes and are regulated by APOE

HFE gene variants, iron, and lipids a novel connection in Alzheimer’s disease.

Diet and Parkinson’s disease I A possiblerole for intake of specific foods and food groups

Vitamin D and Sunlight Exposure in Newly-Diagnosed Parkinson’s Disease.

parkinsons and solanaceum

Dietary fats, cholesterol and iron as risk factors for Parkinson’s disease


Telomeres: You will age faster if you sit around! Telomere length shortens the more sedentary you are – Insane Medicine

  • A great research article in Mayo Clinic Proceedings, marked below, demonstrates the importance of decreasing our sedentary activities. In the study, they determined that telomere length is shortened by sedentary behaviors, measured in the form of leisure-based screen time. Short telomeres is associated with stress, inflammation,  and a variety of cardiometabolic diseases! Short telomeres are an established characteristic of aging. You want to have a successful aging strategy, hence you want to keep your telomeres long! 🙂
  • The measurement of leukocyte telomere length (LTL)  is a method to determine future health, and short LTL is associated with morbidity and mortality independent of age. In the study, 6405 people ages 20-84 were assessed for leisure time screen-based sedentary behavior, namely television, video games and computer use, and a LTL assay was performed on the participants to determine the length of their telomeres over a certain period of time. It was found that for every hour increase in screen based time, the individual had a 7% increased risk of being in the lowest tertile of telomere length. In other words, the more screen based time that was spent, the greater the chance your telomeres were short enough to put you at the bottom of the study group in regards to telomere length.  Hence you have a higher risk of an early illness or death!
  • Physical activity is associated with greater telomere length up to a certain point.
  • The core findings of people with LTL values that were in the bottom group (short telomeres) was that they were more sedentary, engaged in little moderate to vigorous physical activity, had high CRP levels (inflammation marker), had a higher BMI (fatter), and more likely to have diabetes, hypertension, and coronary artery disease.  The chance of a person falling into this category, again increased by 7% for each hour of screen based  leisure time that they spent.
  • Leukocyte telomere shortening is a marker of cellular aging and also is associated with increased morbidity (high blood pressure/diabetes) and mortality. When LTL become critically shortened, the leukocytes secrete pro-inflammatory cytokines and hence increase the CRP ( a marker of inflammation). Thus being sedentary results in inflammation and modulates your metabolic risk in the wrong direction.  In other words, you age faster!!!
  • The key point: Stay active physically and spend less time on Facebook!!
  • Leisure-Time Screen-Based Sedentary Behavior and Leukocyte Telomere Length: Implications for a New Leisure-Time Screen-Based Sedentary Behavior Mechanism –  Paul Loprinzi

Leisure-Time Screen-Based Sedentary Behavior and Leukocyte Telomere Length: Implications for a New Leisure-Time Screen-Based Sedentary Behavior Mechanism


Other interesting abstracts:

Bey, L. and Hamilton, M.T. Suppression of skeletal muscle lipoprotein lipase activity during physical inactivity: a molecular reason to maintain daily low-intensity activity. J Physiol. 2003; 551: 673–682

Suppression of skeletal muscle lipoprotein lipase activity during physical inactivity: a molecular reason to maintain daily low-intensity activity  Bottom line of article:  Inactivity caused a local reduction of plasma [3H]triglyceride uptake into muscle and a decrease in high density lipoprotein cholesterol concentration. Treadmill walking raised LPL activity approximately 8-fold (P < 0.01) within 4 h after inactivity The striking sensitivity of muscle LPL to inactivity and low-intensity contractile activity may provide one piece of the puzzle for why inactivity is a risk factor for metabolic diseases and why even non-vigorous activity provides marked protection against disorders involving poor lipid metabolism.

Tremblay, M.S., Colley, R.C., Saunders, T.J., Healy, G.N., and Owen, N. Physiological and health implications of a sedentary lifestyle. Appl Physiol Nutr Metab. 2010; 35: 725–740  Sedentarism, active lifestyle and sport: impact on health and obesity prevention

The benefits of regular physical activity have been known since ancient Greek. But in the last Century the scientific knowledge around this topic has progressed enormously, starting with the early studies of JN Morris and RS Paffenberger, who demonstrated that physical activity at work reduced incidence of cardiovascular disease and mortality. In the Harvard alumni study, the lowest risk was associated with a weekly output of 1000 to 2000 kcal performing vigorous activities. Further studies in all age groups have supported these findings and have added that even moderate levels of physical activity provide considerable benefits to health, including lower prevalence of overweight and obesity at all ages. Metabolic fat oxidation rate is highest at exercise intensities between 45 and 65% of VO2max. This means that people must be active regularly and force physiological mechanisms at certain intensities. All this body of evidence has contributed to current WHO physical activity recommendations of 150 min/week of moderate to vigorous physical activity (MVPA) in adults and elderly, and 60 min/day of MVPA in children and adolescents, with additional strength training, apart from adopting an active lifestyle. In the last 50 years, occupational physical activity has been reduced for about 120 kcal/day, and sedentarism has emerged as an additional risk factor to physical inactivity. Even if less than 60 min of TV time in adults have been related to lower average BMI, there is still a need for research to determine the appropriate dose of exercise in combination with sedentary behaviours and other activities in the context of our modern lifestyle in order to prevent obesity at all ages. As public health measures have failed to stop the obesity epidemic in the last 3 decades, there is clearly a need to change the paradigm. The inclusion of sport scientists, physical education teachers and other professionals in the multidisciplinary team which should be responsible for drawing the road map to prevent the increase of the obesity epidemic effectively is a “must” from our point of view.


Physical inactivity as the culprit of metabolic inflexibility: evidence from bed-rest studies

Bergouignan, A., Rudwill, F., Simon, C., and Blanc, S. Physical inactivity as the culprit of metabolic inflexibility: evidence from bed-rest studies. J Appl Physiol (1985). 2011; 111: 1201–1210


The following sequence of events can be hypothesized to explain the physical inactivity-induced metabolic alterations and thus metabolic inflexibility (Fig. 4). The physical inactivity induced by bed rest leads to insulin resistance in skeletal muscle, requiring a hyperinsulinemic response to properly dispose of glucose in daily postprandial conditions, whereas adipose tissue displays an appropriate response. At the same time, muscle fiber type shifts toward fast-twitch glycolytic fibers, and muscle increases glucose uptake and oxidation through insulin-independent pathways. This in turn inhibits fatty acid oxidation and ultimately uptake. During meal ingestion, hyperlipemia occurs due to a decreased plasma clearance of dietary fat. This increases the flux of dietary lipids to organs and results in ectopic fat storage with consequences on insulin sensitivity. The liver displays susceptibility to hyperinsulinemia and increased lipid synthesis and storage that overcomes rate of oxidations. Hepatic steatosis will likely ensue. With a reduced oxidative capacity, the liver will then contribute to an increased rate of atherogenic lipid products (VLDL) in which the contributions of FFA coming from the diet and neolipogenesis to the total VLDL-triglycerides will increase, feed-forwarding hyperlipemia and ectopic fat storage. Concomitantly, the steatotic liver will become insulin resistant and unable to suppress hepatic glucose production, which leads to increased gluconeogenesis and feed-forward worsening of hyperinsulinemia.Inactivity and metabolic inflexibilityHypothetical metabolic alterations cascade induced by bed rest that can explain how physical inactivity induces metabolic inflexibility. VLDL, very-low-density lipoprotein; NAFLD, nonalcoholic fatty liver disease; DAG, diacylglycerol.

Physical activity predicts metabolic flexibility. For an equivalent food quotient, metabolically flexible subjects will greatly increase carbohydrate oxidation after the consumption of a meal despite a low increase in plasma insulin concentration. A metabolically inflexible individual, i.e., a person who also displays an insulin resistance, will display a low increase in carbohydrate oxidation despite an marked elevation in insulin secretion.

Weischer, M., Bojesen, S.E., Cawthon, R.M., Freiberg, J.J., Tybjӕrg-Hansen, A., and Nordestgaard, B.G. Short telomere length, myocardial infarction, ischemic heart disease, and early death. Arterioscler Thromb Vasc Biol.2012; 32: 822–829

Short Telomere Length, Myocardial Infarction, Ischemic Heart Disease, and Early Death  -> Findings: Short telomere length is associated with only modestly increased risk of myocardial infarction, ischemic heart disease, and early death.

Leucocyte telomere length and risk of cardiovascular disease: systematic review and meta-analysis BMJ 2014;349:g4227 Available observational data show an inverse association between leucocyte telomere length and risk of coronary heart disease independent of conventional vascular risk factors. The association with cerebrovascular disease is less certain.

Chronic inflammation induces telomere dysfunction and accelerates ageing in mice  Our results show that chronic inflammation aggravates telomere dysfunction and cell senescence, decreases regenerative potential in multiple tissues and accelerates ageing of mice. Anti-inflammatory or antioxidant treatment, specifically COX-2 inhibition, rescued telomere dysfunction, cell senescence and tissue regenerative potential, indicating that chronic inflammation may accelerate ageing at least partially in a cell-autonomous manner via COX-2-dependent hyper-production of ROS.

Cawthon, R.M. Telomere measurement by quantitative PCR. Nucleic Acids Res. 2002; 30: e47   Telomere measurement by quantitative PCR



Insane Medicine – Blood Markers for Alzheimer’s Disease

  • A recent paper listed below studied the presence of autolysosomal proteins (from nerve tissue exosomes) in the blood stream and found a very high correlation with the eventual appearance of Alzheimer’s disease some ten years before it is detectable clinically.
  • Cathepsin D, LAMP-1 (lysosome-associated membrane protein 1), and ubiquitinylated protein were higher in patients who developed Alzheimer’s disease whereas Heat-Shock protein 70 was lower.
  • These markers confirm neuronal lysozomal dysfunction years in advance of Alzheimers and these markers may be used as biomarkers of disease.
  • Altered lysosomal proteins in neural-derived plasma exosomes in preclinical Alzheimer disease
  • Neurology. 2015 Jun 10.

Insane Medicine – Cardiac Rehabilitation will save your life

Cardiac rehab and healthy eating save lives
Cardiac rehab and healthy eating save lives!

eat healthy

  • Have you had a heart attack? Then why aren’t you in cardiac rehab if your doctor says it’s okay?
  • Those who are involved in cardiac rehab have a 47 % decrease in heart attack risk over the next two years! Also, those who participate have fewer hospital admissions and live longer.
  • Cardiac rehab is an option post-heart attack, as well as for those with arrhythmias and heart failure. It is associated with decreased mortality and prolonged survival.
  • Cardiac Rehab is coached by trained professionals who teach you how to appropriately exercise based on your capabilities and prescription. This improves your functional status.
  • It also involves nutritional counseling, teaching the patient to eat a low fat and sodium diet to help manage cholesterol levels and blood pressure. This allows you to maintain a healthy weight.
  • cardiac rehab also helps you maintain a regimen. More important, one must take their prescribed medications for optimal outcomes. Compliance leads to success. Education about medications that are important is a key  factor.
  • Cardiac rehab also educates one to avoid unhealthy habits, such as smoking and maintaining diet. likewise, the mental aspect of a post-cardiac condition is crucial in maximizing outcomes. Depression and other mental disorders must be fully addressed and treated.
  • Exercise creates stronger muscles and improved cardiovascular fitness that improves ones emotional state as well. Cardiac rehab must be continued in the home environment for maximal impact.
  • The journal BMJ showed that even a little bit of exercise provides noticeable benefits of health. the goal is 150 minutes of exercise per week, but even small amounts of physical activity may decrease the mortality risk.
  • Exercise helps with depression and boosts your natural endorphins that make you feel better, resulting in increased energy levels. Exercise allows you to take control of your life and is a mood enhancer that gives you an overall sense of well-being.
  • Depression and anxiety can be blunted by such exercise programs, especially when they are maintained at home as well. Meditation and behavior modification are key components to creating a healthy lifestyle. People who are depressed and feel hopeless have a higher rate of dying from their cardiac disease. exercise at least 30 minutes a day, working your way up to that amount even if you don’t have the internal motivation to do so.

Insane Medicine – Acid in our bodies is a problem – Metabolic acidosis (MA)

Acid is not good
Acid is not good

acid house acid mushroom

  • Our bodies are always in a battle with too much ACID. I discussed this briefly before and am revisiting this topic again because of the metabolic impact metabolic acidosis (MA)  has on our bodies (that is, too much acid)
  • In the process of digesting meats and animal proteins, our body produces acids as well as internal processes that contribute to high acid levels. Our body uses bicarbonate and other  mechanisms to neutralize the excess acid.
  • Metabolic acidosis (MA) affects every system in our body. MA at a chronic level activates bone resorption and can increase the rick of osteoporosis. Treatment of MA can decrease this risk when it is present. Skeletal strength is impaired by MA because the body cannibalizes it’s own muscle to help neutralize the extra acid. Likewise, MA will impair insulin release and insulin receptor functioning. This results in glucose intolerance and diabetes. MA will also cause the progression of kidney failure and impair the functioning of thyroid hormones and it’s receptors.
  • We see metabolic acidosis in 1 out of 30 patients with normal  kidney function. the number affected increases as kidney function declines.
  • BMC Nephrol, 2013 Jan 9;14:4 : Use of bicarbonate to normalize MA can prevent progression of chronic kidney disease. How much bicarbonate and what type of bicarbonate is used? Sodium bicarbonate, in amounts starting at 1300 mg twice a day to get the serum bicarbonate levels to 24 mg/dl. Baking soda has 850 mg of sodium bicarbonate in a teaspoon.
  • Sodium bicarbonate intake does not worsen high blood pressure because the sodium load resulting from the sodium bicarbonate cannot be reabsorbed in the kidney through the usual NACL cotransporter.
  • The body normally excretes extra acid loads produced in the body in the form of ammonia, which is produced from glutamine (an amino acid) When metabolic acidosis is present, the body quickly runs out of glutamine from its usual sources and gets extra glutamine from muscle breakdown. The glutamine then goes to the kidney to be broken into ammonia which absorbs the extra acid.  So metabolic acidosis leads to increased muscle breakdown and weakness.
  • Diet affects the production of acid, especially with the consumption of animal proteins, which results in a lot of acid production in the body. This speeds UP the loss of kidney function in predisposed individuals. It has been shown that fruits and vegetables create little acid production in the body and a vegan diet as such decreases the rate of kidney function decline in patients with kidney failure.


Here is the summary:

  1. Treatment of metabolic acidosis, when the serum bicarbonate level is below 20 mmol/L, using sodium bicarbonate at doses of 1300 mg twice a day to increase serum bicarbonate to 24 mmol/L has positive impacts in multiple fronts as below.
  2. Increased bone density results from treatment of MA, thus decreased fractures and falling.
  3. There is better glucose control by treating MA due to better insulin sensitivity and insulin receptor responsiveness.
  4. Treatment of metabolic acidosis decreases the progression towards kidney failure in susceptible individuals with chronic kidney disease.
  5. Treatment of MA results in better muscle strength and muscle mass.
  6. Eat more fruits and vegetables to decrease your intake of acids.
  7. Have your doctor asses your blood for low bicarbonate (Less than 20 mmol/L)
  8. Consult your doctor prior to initiating any medical regimen as discussed.

Insane Medicine – Sedentary Behavior is a disease!

Keep active
Keep active
  • Study after study documents the same finding: Regular physical activity at ANY age plays the major role in maintenance of brain functioning and health. Even if you have been inactive for years, you can benefit by slowly initiating a physical activity program.
  • Sedentary behavior is the enemy. When you exercise, you must  also decrease sedentary behavior throughout the day as well to obtain maximum benefit.
  • Sedentary behavior causes damage to the brain’s structure and per a study in PLOS ONE (9/2014), age-related changes in the brain were more prominent in the hippocampus region (memory-making center of the brain) in patients who were sedentary. Sedentary behavior ROTS your brain!
  • Brain plasticity, the brain’s ability to make new connections in response to it’s environment, is improved with physical activity and exercise. What results is better memory and decision-making skills. This can decrease brain atrophy. On CT scans of the brain, many elderly patients demonstrate shrunken brains, much of which can be reduced by physical activity. Additional benefits of brain-preservation outside of better memory and attention is a positive effect on mood and stress. Physical activity can lower blood pressure, control blood sugar, and reduce obesity, all of which negatively impacts brain functioning.
  • What type of exercises should one do? Aerobic exercises, resistance exercises, and gross motor activities. Again, aerobic activities of 30 minutes a day for 5 out of 7 days a week are an excellent goal. Consider jogging, swimming, tennis, dancing, stair climbing, and bicycling for aerobic activities. Build up your muscles with resistance training such as sit ups, weight lifting, and leg raises. The goal is at least three sessions a week to increase muscle tone and strength, which also helps with balance.  Consider Yoga and Tai Chi to help with movement, balance, and flexibility. Balance and strength are very important to decrease falling risks. In fact, there are numerous studies documenting the positive benefit of Tai Chi on decreasing the rate of falling in elderly people.
  • Between exercising sessions, don’t just sit around – KEEP MOVING! Non-exercise physical activity, such as gardening, laundry, dish washing, and climbing the stairs can add to physical and brain health. These activities help maintain mobility  (American Journal of Preventive Medicine). This type of activity complements the other exercise components. This type of activity can reduce heart attack risk and stroke risk by improving weight as well as lipid levels.

Insane Medicine – Even older people should watch their diet

Successful aging requires continued effort for the best outcome. Do you want to live to one hundred and be bed-bound or live to one hundred and be active? Successfully aging people need to consider healthful behaviors to maintain their independence and health. Conditions that affect people over sixty can be modified and lessened by nutritional strategies:

  1. Cardiovascular diseaseHigh blood pressure, cholesterol/triglycerides, and obesity are modifiable by diet and medication. Weight control allows for better mobility, less pain, and fewer heart attacks. Obesity is associated with sleep apnea, as well, which reduces quality of life because it makes you fatigued in the day time and generally weak.
  2. Cerebrovascular Disease: Such as strokes and dementia are impacted by high blood pressure and diet. First off, quit smoking to decrease your risk of dementia and stroke. Decrease your sodium intake to decrease your blood pressure (1500 mg of sodium a day is about right for an average diet.) Use herbs and spices to flavor your foods. Foods such as cold cuts, cheeses, breads, pizza, pasta dishes, snack foods, and soups have higher levels of sodium, so beware. Consider following the DASH diet:  and 
  3. Diabetes Control: Diabetes affects everything from your eyes to your kidneys. There is a four-fold increased risk of death from heart disease or stroke if you are diabetic. Take your medicines, track your hemoglobin A1C (sugar control measure) and eat  food with a low glycemic index. Eat food with less fat and avoid high-sugar content items, but include more vegetables and whole grains to maintain glucose control. It takes a lot of effort if you are diabetic, so don’t let diabetes take your life one leg at a time!
  4. Cancer: Get your recommended screening examinations. Also, maintain a healthy weight since obese people have higher risks of cancer!
  5. Chronic Kidney Disease: Another disease modifiable by diet control – CKD risk is increased if you have hypertension, diabetes, obesity, or cardiovascular disease. A healthy diet and physical activity will maintain your weight and blood pressure, minimizing aging’s impact on your kidneys!


  • Eat bright colored vegetables (carrots, brocolli) and deep colored fruits (berries) for phytochemical, healthy support.
  • Chose whole, enriched, fortified grains and cereals, i.e. whole wheat bread.
  • Chose low and non-fat dairy products: Yogurt and low-lactose milk
  • Use herbs and spices to add flavors to meals
  • Lots of fluids: no sodas
  • Exercise

Insane Medicine – Lowering Dementia Risk


Research is demonstrating that treating multiple risk factors for dementia results in better outcomes than treating each factor individually. Risk factors include:

  1. Poor nutrition
  2. obesity’smoking
  3. physical inactivity
  4. cardiovascular risks
  5. depression
  6. social isolation
  7. lack of mental stimulation

Strategies to help deal with these risks have been shown to help improve cognitive performance. Just treating single variables such as high blood pressure or lack of exercise has less effect than hitting multiple factors at once. A study in Lancet Neurology (August 2014) revealed that one-third of Alzheimer’s Disease (AD) cases are attributable to modifiable factors and thus AD may be reduced in prevalence by improved education , treatment of depression, and management of vascular risk factors such as physical inactivity, smoking, hypertension, obesity, and diabetes.

  • Get regular exercise: this reduces stress, improves blood flow to the brain, strengthens connection of neurons in the brain, improves medical health and balance, thus reducing falls. The goal is 30 minutes of aerobic activity five times a week (walking, dancing, biking as examples) and strength training twice a week.
  • Challenge your brain: Demanding brain activities utilizing different aspects of your intellect help protect against cognitive decline, making your mind more efficient and able to focus. So expose yourself to new ideas and challenges mentally, so that you can maintain your memory skills and concentration abilities. Things like cross-word puzzles, checkers or cards help build up your brain as do math problems. Research shows that staying intellectually engaged may prevent AD. These types of brain challenges add to your cognitive reserve. Social interaction also plays a role in preventing cognitive decline. It has been found that those who play more games or puzzles were more likely to perform better on test of memory, learning, and information processing. They also have greater brain volume in areas associated with memory. Mental workouts enhance brain blood flow and promote cell growth, stronger neuron connections, and keep the brain efficient. It makes the brain less sensitive to trauma such as drugs, stroke, or disease. The internet has resources to help:  or  or  or  or   So consider crossword puzzles, jigsaw puzzles, word searches, math problems, an brainteasers to exercise your mind!
  • Treat mental illness, especially depression: Sadness, hopelessness, and lack of energy may signal depression. Depression is associated with a high risk of cognitive decline. See your doctor to help get treatment.
  • Eat a healthy diet: Eat complex carbohydrates such as whole grains, legumes, fruits, and vegetables. Avoid sodas, sweets, and excess sugars. Protein is essential for growth and cell maintenance, so consider lean meats, fish, poultry, eggs, low fat dairy,  nuts, and beans. Chose healthy fats such as omega-3 fatty acids found in flaxseed oil, fish, and nuts. Monounsaturated fats are also healthful and is present in olive and canola oils. Polyunsaturated fats from corn, safflower, and sunflower seeds are fine as well. Avoid trans-fats. Remember to include your micronutrients and phytochemicals (found in plant sources).
  • Treat cardiovascular risks: Stop smoking, lose weight, be physically active, treat high blood pressure and diabetes, take your prescribed medications.

Avoid Trans-fats in your diet. It is found in many junk foods, especially fast foods, processed foods, baked goods, margarine, and other sources. These products and trans-fats perform about 10% worse on cognitive tests than those who consumed minimal amounts. Trans-fats promote oxidative stress and damage the memory center of the brain, the hippocampus.

Magnesium is essential for brain functioning. It is found in green leafy vegetables, whole grains, nuts, legumes, and hard water. Magnesium helps in energy production, needed especially in the brain. It helps in the formation and release of neurotransmitters as well as functioning of connections in the brain (synapses) to process new information. Studies in Molecular Brain (September 2014) demonstrated that magnesium L-threonate (MgT) supplementation prevented memory decline and prevented synapse loss in mice prone to AD. It also reduced the deposition of beta-amyloid protein in the brain (a cause of AD) Risk factors for magnesium depletion include chronic alcoholism, diabetes, excessive coffee intake, inflammatory bowel disease such as Chrone’s disease, diuretic intake, liver and kidney disease,  and excessive soda and salt intake.The RDA is 400 mg a day –  This link points to sources of magnesium for your diet. Foods included are Almonds, spinach, cashews, peanuts, shredded wheat cereal, soy milk, black beans, whole wheat bread, avocado, baked potato, brown rice, plain yogurt, and others.

This sounds dumb but avoid head injury – it has been shown that older adults who have a head injury are at higher risk of dementia, especially over the age of 65. The main reason for these injuries are falls, many of which are preventable and may be due to deconditioning and weakness from lack of exercise. Remember that exercise increases strength and balance.

Remember to not be anxious over your health – don’t become a hypochondriac. Maintain your health through proper eating, exercise, risk management of cardiovascular problems (high blood pressure, high cholesterol, smoking cessation), taking your prescribed medications, and regular physician check-ups will maximize your health. Don’t get preoccupied with health matters and fears of disease such that they interfere with your daily activities and enjoyments in life. Keep yourself busy and distracted by learning new tasks and volunteering. Consider meditation, relaxing your body and mind, concentrating on the present moment. Exercise your body to reduce stress and reduce your anxiety. This will build your physical strength and increase your feelings of well-being. Keep your head up with positive feeling and be grateful for the good things in your life and those things you can control. Don’t stress out!!




Insane Medicine – Running beats walking in older adults!

Insane Medicine - Running beats walking in older adults
Insane Medicine – Running beats walking in older adults.
  • Research has indicated that running may lead to better outcomes in older adults. A study by Orteg JD et al in PLoS One (2014;9:e113471) compared walking and running in older adults.  Basic tasks begin to deteriorate in older adults, including the basic ability to walk. The economy (metabolic expenses) of walking get worse as one ages due to muscular inefficiency and the firing of antagonistic muscle groups in older muscle. This increases the risk of falling, and also increases the difficulty of basic transferring of weight from one point to another as well as maintaining balance.
  • In other studies, it has been found that older runners have a similar running economy as younger runners do. This new study in PLoS One demonstrates that older runners have more efficient energy use when they walk as compared to non-runners at the same age. In fact, the gross metabolic cost of transport was about 10 % less in runners at any walking speed.
  • Older walkers walkers are not able to stop the deterioration in the metabolic cost of walking because they have the same metabolic cost of transport as older sedentary adults.  All exercise is not the same for all people!
  • Key Point: There are benefits to a regular running practice in older adults in regards to longevity and overall health. In fact, older adults who run at least 30 minutes three times a week have less metabolic cost for walking than individuals of the same age group who exercise by walking only! Thus running improves your metabolic efficiency and prevents age-related declines in walking efficiency!
  • Intense training in older adults increases muscular efficiency and stops antagonistic muscle firing.
  • CDC recommendation for physical activity link:
  • Government recommendation for physical activity:   and