Let’s Talk about Gut Health and Probiotics with Marisa Moore, RDN

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Let’s Talk about Gut Health and Probiotics with Marisa Moore, RDN
Marisa Moore, MBA, RDN, LD

What is gut health?

Gut health has become a buzzword over the past decade. Over the years, recognizing the importance of gut health has gone from simply focusing on what we eat and digestion to its impact on overall wellness.

But let’s back up a bit to understand why. The gastrointestinal tract (or GI tract) is essential for moving food from the mouth throughout the body, converting that food into nutrients our body can absorb, and eliminating waste.1 However, the GI tract is more than a pathway for absorbing nutrients. Its health can impact the entire body.

Growing research suggests that gut health goes well beyond good digestion.2 It may have an impact on the immune system and mood.3-5 Research on gut bacteria continues to grow and may be a key factor in understanding and maintaining gut health.

Disruptions to the GI Tract

Dietary and lifestyle patterns can affect the GI tract.

Gut microbiota—the microbe population living in the intestines—is sensitive to a variety of factors including lifestyle, dietary patterns, environmental factors and aging.6 Temporary changes like travel can have an impact. But daily habits have the greatest influence over time. Changes in what you eat—particularly food quality and excessive alcohol intake—significantly affect gut symbiosis7; that is, how your gut bacteria get along and maintain balance.

Skimping on fruits and vegetables may starve gut bacteria and affect their ability to thrive. As such it’s important to provide gut bacteria with a constant supply of fuel for optimal balance and health.

There’s now evidence that the Western-type diet—higher in fat and lower in fiber—can result in a shift in the microbial balance of the gut. Researchers are also studying how ultra-processed foods might affect gut. On the other hand, a diet high in sources of complex carbohydrates and fiber, such as legumes, fruits and vegetables and whole grains, can support the growth of healthy microbial populations.8,9

Further, there’s some evidence that our gut microbes affect sleep and might influence our circadian rhythm. The gut microbiome plays a key role in many different body systems. When it’s out of balance, we might experience sleep disturbances and become more susceptible to stress. Evidence suggests that the relationship between circadian rhythm and the gut microbiome may be bidirectional. 10 Though research exploring the gut-brain connection is in its infancy and largely based on animal models, it may shed light on how an imbalance in the microbiome might impact our mood, sleep, and mental health.11

What are Probiotics?

Probiotics are microorganisms that may provide a health benefit upon ingestion. These beneficial bacteria help us absorb nutrients and fight off unwanted bacteria in the gut. You can get probiotics from food or supplements.12

Getting probiotics regularly may help you establish more healthy bacteria in the gut. And that comes with benefits. Research suggests that probiotics offer strain-specific health benefits. These include a potential positive impact on the immune system, bowel regularity, mood and more.2

That’s probiotics. But what about prebiotics?

Prebiotics help feed gut bacteria. Prebiotics are largely indigestible carbohydrates or fibers found naturally in certain foods including chicory root, sunchokes (or Jerusalem artichokes), bananas, garlic, onions, asparagus and oats. Prebiotics are fermented in the gut to help gut bacteria thrive.

An easy way to remember the difference is that prebiotics are food for the friendly bacteria in the gut.13,14

Probiotics and Nutrition

Yogurt, kefir and pickled vegetables like kimchi and sauerkraut are a few top food sources of probiotics. For a daily dose of probiotics, you might enjoy Greek yogurt and fresh fruit for a snack or try kefir in a breakfast smoothie to effortlessly add probiotics to your morning routine.

If you’re curious about how to get the most bang for your bite, there are a few things to consider.

  • Look for yogurt and kefir with live and active cultures. It’s often noted on the packaging. And try to eat the yogurt sooner than later since the number of cultures may decline over time depending on storage conditions and packaging.15
  • Though pickled vegetables contain some probiotics, it’s often difficult to determine just how much. Plus, pasteurized fermented foods may not have as many probiotics as those that are not.

Healthful diet with probiotic supplementation

Different probiotic supplements offer different potential benefits.

Benefits may be strain-specific. That is, the type of probiotic supplement you take should contain strains supported by research.

Remember that not all probiotics are created equal. This means that one Lactobacillus supplement is not necessarily like another. From differences in potency to manufacturing practices and storage, and the research backing up the specific strains they use, supplements vary. Choose products supported by clinical research and opt for a high-quality supplement brand you trust.

FLORASSIST® GI with Phage Technology

Studies show that gut health is influenced by a number of factors. Probiotic supplements may help to have a healthy and protective balance. Technological innovations are making this even easier.

You have to do your research to find the right products. And since you’re here, you’ve already taken the first step.

Life Extension offers several FLORASSIST® probiotics, each with its own health benefits. Life Extension FLORASSIST® with Phage Technology combines potent probiotics with innovative bacteriophage technology and takes a dual-action approach to support gut health.
Here are the top benefits at a glance:

  • Probiotic blend with 15 billion colony forming units (CFU)
  • Innovative TetraPhage Blend affects unwanted bacteria
  • Supports the growth of probiotic bacteria
  • Promotes digestion and stomach health

You can take comfort in knowing that the Phage technology is designed to only affect undesirable bacteria, leaving your existing good bacteria to thrive and create the ideal balance in your gut.

Synergy: supplements and a healthy diet

We know that a healthy diet is a key to lifelong health. But sometimes you need a little help. And some strains can help support the immune system from seasonal immune challenges.19 These are a few ways to use supplements to complement a healthy diet. And eating probiotic-rich foods doesn’t keep you from also incorporating supplements.

When transitioning from a heavily processed diet to incorporate more whole foods, take a small step approach. Going too fast can be overwhelming and may lead you to just give up. Think about what you can add to make it easier. Try pre-chopped or frozen vegetables for a dinnertime shortcut. Add big handfuls of spinach to a pasta dish or try healthy dishes when you’re out to eat. If, for example, you’re a big macaroni and cheese fan, add in some chopped cauliflower for a vegetable boost.

The Bottom Line

The best way to maintain a healthy gut microbiome is through a healthy whole foods diet including plenty of probiotic- and prebiotic-rich foods. Probiotic supplements can help complement this diet to improve gut health and other parts of the body as well.

About the Author: Marisa Moore, MBA, RDN, LD is a nationally recognized registered dietitian nutritionist and communications and culinary nutrition expert. Her integrative and practical approach to providing healthy and delicious recipes coupled with science-based nutrition advice is regularly featured in the nation’s leading media outlets including CNN, the TODAY Show, Dr. Oz. Show, Women’s Health, Prevention, and many more. She is a consultant to food and nutrition companies, contributing editor for Food and Nutrition Magazine, contributor to People magazine and other national publications. Before launching her consultancy, Marisa worked as an outpatient dietitian, corporate nutritionist for a restaurant chain, and she managed the employee worksite nutrition program at the U.S. Centers for Disease Control and Prevention (CDC). Connect with Marisa at https://marisamoore.com.




References:

  1. National Institute of Diabetes and Digestive and Kidney Diseases. Your Digestive System & How it Works. https://www.niddk.nih.gov/health-information/digestive-diseases/digestive-system-how-it-works. Updated 12/2017. Accessed 10/8/2019.
  2. Khanna S, Tosh PK. A clinician’s primer on the role of the microbiome in human health and disease. Mayo Clin Proc. 2014;89(1):107-114.
  3. Hemarajata P, Versalovic J. Effects of probiotics on gut microbiota: mechanisms of intestinal immunomodulation and neuromodulation. Therapeutic advances in gastroenterology. 2013;6(1):39-51.
  4. Huang TT, Lai JB, Du YL, Xu Y, Ruan LM, Hu SH. Current Understanding of Gut Microbiota in Mood Disorders: An Update of Human Studies. Front Genet. 2019;10:98.
  5. Liu L, Zhu G. Gut-Brain Axis and Mood Disorder. Frontiers in psychiatry. 2018;9:223.
  6. Hasan N, Yang H. Factors affecting the composition of the gut microbiota, and its modulation. PeerJ. 2019;7:e7502.
  7. Mutlu EA, Gillevet PM, Rangwala H, et al. Colonic microbiome is altered in alcoholism. American journal of physiology Gastrointestinal and liver physiology. 2012;302(9):G966-978.
  8. Martinez KB, Leone V, Chang EB. Western diets, gut dysbiosis, and metabolic diseases: Are they linked? Gut Microbes. 2017;8(2):130-142.
  9. Zinocker MK, Lindseth IA. The Western Diet-Microbiome-Host Interaction and Its Role in Metabolic Disease. Nutrients. 2018;10(3).
  10. Li Y, Hao Y, Fan F, Zhang B. The Role of Microbiome in Insomnia, Circadian Disturbance and Depression. Frontiers in psychiatry. 2018;9:669.
  11. Foster JA, Rinaman L, Cryan JF. Stress & the gut-brain axis: Regulation by the microbiome. Neurobiology of stress. 2017;7:124-136.
  12. National Center for Complementary and Integrative Health. Probiotics: What You Need To Know. https://nccih.nih.gov/health/probiotics/introduction.htm. Updated 8/2019. Accessed 10/8/2019.
  13. Ferrario C, Statello R, Carnevali L, et al. How to Feed the Mammalian Gut Microbiota: Bacterial and Metabolic Modulation by Dietary Fibers. Front Microbiol. 2017;8:1749.
  14. Davani-Davari D, Negahdaripour M, Karimzadeh I, et al. Prebiotics: Definition, Types, Sources, Mechanisms, and Clinical Applications. Foods. 2019;8(3).
  15. Ferdousi R, Rouhi M, Mohammadi R, Mortazavian AM, Khosravi-Darani K, Homayouni Rad A. Evaluation of probiotic survivability in yogurt exposed to cold chain interruption. Iranian journal of pharmaceutical research : IJPR. 2013;12(Suppl):139-144.
  16. McFarland LV, Evans CT, Goldstein EJC. Strain-Specificity and Disease-Specificity of Probiotic Efficacy: A Systematic Review and Meta-Analysis. Front Med (Lausanne). 2018;5:124.
  17. Issa I, Moucari R. Probiotics for antibiotic-associated diarrhea: do we have a verdict? World J Gastroenterol. 2014;20(47):17788-17795.
  18. McFarland LV. Meta-analysis of probiotics for the prevention of antibiotic associated diarrhea and the treatment of Clostridium difficile disease. The American journal of gastroenterology. 2006;101(4):812-822.
  19. Yang G, Liu ZQ, Yang PC. Treatment of allergic rhinitis with probiotics: an alternative approach. North American journal of medical sciences. 2013;5(8):465-468.

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Cycles of DNA Damage and Repair as a Cause of Age-Related Epigenetic Drift

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Researchers have recently proposed that the normal operation of DNA repair contributes to the epigenetic change that is observed to occur with age. This is an interesting concept, and we’ll see how it progresses in the years ahead, particularly as therapies based on alteration of epigenetic markers emerge as an area of active medical research and development.

Epigenetic decorations to DNA are a part of the complex regulatory system controlling the amounts and timing of protein production carried out by a cell. Cells react to changing circumstances with changes to epigenetic markers such as DNA methylation. Some of the alterations in cells and tissues that take place with advancing age, such as rising levels of molecular damage, are very similar between individuals, and thus weighted combinations of the status of specific epigenetic markers can be used to measure age. But most epigenetic change is highly variable and highly individual, dependent on the circumstances that each cell finds itself in, communications with surrounding cells, the overall environment, diet, state of health, and so forth.

At the present time is far from clear as to why exactly most epigenetic changes occur; building the full map and understanding of epigenetic adjustments in response to circumstances will likely still be a going concern decades from now. Even those epigenetic markers used to build biomarkers of aging are not yet firmly connected to specific underlying causes, though work is proceeding towards that end. This uncertainty gives rise to academic and popular debate over where epigenetic change sits in the tangled web of cause and consequence in aging. Programmed aging theorists hold that epigenetic changes are a cause of aging, and reversing them is therefore rejuvenation. Aspects of this view are being voiced more loudly these days, now that certain entities with deep pockets and well-oiled hype machinery are putting venture funding into the development of clinical therapies based on reprogramming cells to have youthful epigenetic patterns.

It would be very surprising to find that epigenetic change is at the roots of aging. The most telling arguments against this are the numerous contributions to aging based on the accumulation of metabolic waste that our biochemistry cannot break down, even in youth. No approach to restoring youthful epigenetic patterns can address that. Epigenetic change can certainly be a proximate cause to all sorts of disarray in aging, however. Reprogramming cells has been shown to restore mitochondrial function, and the general malaise in mitochondria that takes place in all cells in aging tissue can be traced back through failing fission, failing mitophagy, to gene expression levels of specific proteins. Force a cell to produce those proteins at a youthful level, and mitochondria will function once again.

Yet how great a gain can be produced while ignoring the underlying causes? If the history of medicine teaches us anything, it is that efforts to treat age-related disease without addressing its causes have been a miserable failure. Will it really be that much better to take one or two steps closer to the cause, while still not addressing it? That is an important question, and one we are going to see tested in practice, sadly. Enthusiasm and funding for taking those one to two steps is far greater than that for addressing the known root causes of aging.

In this broader context, the work noted here is quite interesting, proposing that the normal ongoing processes of DNA damage and repair taking place in every cell can, over time, produce at least some of the epigenetic changes of aging. They use artificially raised levels of DNA damage and repair to produce accelerated epigenetic change in mice that is at least similar to that of aging.

DNA Damage Leads to Epigenetic Alterations


Despite it long having been the consensus that DNA damage and the resulting epigenetic changes are drivers of aging, some recent studies have questioned the importance of mutations in aging. For example, the number of mutations present in aged yeast cells is fairly low, and some genetically engineered strains of mice with high levels of free radicals or mutation rates do not appear to age prematurely, nor do they have shorter lifespans than their wild-type counterparts.

This appears to suggest that mutational load may not have such a strong influence on aging as was once thought, and the researchers of this new study consider further evidence suggesting the same. They also suggest that epigenetic alterations are perhaps the most important driver of aging and that, far from being random in nature, these changes are predictable and reproducible.

Researchers suggest that DNA double-strand breaks (DSBs) are a possible reason for epigenetic changes and show that there are clues to be found in yeast. In yeast cells, DSBs trigger a DNA damage signal that summons epigenetic regulators and takes them away from gene promoters to the site of the DSB on the DNA, where they then facilitate the repair of the break. The researchers suggest that after these repairs, the regulators responsible for repairing the DSBs return to their original locations on the genome, thus turning off the DNA damage signal, but this does not always happen.

The researchers suggest that with each successive cycle of DNA damage response and repair, the epigenetic landscape begins to change and regulators gradually become displaced, reaching a point where the DNA damage response remains active, leaving cells in a chronic state of stress. This stressed state then causes them to become dysfunctional and ultimately alters their cellular identity.

DNA Break-Induced Epigenetic Drift as a Cause of Mammalian Aging


There are numerous hallmarks of aging in mammals, but no unifying cause has been identified. In budding yeast, aging is associated with a loss of epigenetic information that occurs in response to genome instability, particularly DNA double-strand breaks (DSBs). Mammals also undergo predictable epigenetic changes with age, including alterations to DNA methylation patterns that serve as epigenetic “age” clocks, but what drives these changes is not known. Using a transgenic mouse system called “ICE” (for inducible changes to the epigenome), we show that a tissue’s response to non-mutagenic DSBs reorganizes the epigenome and accelerates physiological, cognitive, and molecular changes normally seen in older mice, including advancement of the epigenetic clock. These findings implicate DSB-induced epigenetic drift as a conserved cause of aging from yeast to mammals.

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Becoming Overweight Raises the Risk of Many Cancers

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People who become overweight at younger adult ages have significantly greater cancer risk than their slimmer peers. Visceral fat tissue is very active, producing chronic inflammation through a range of mechanisms including the production of greater numbers of lingering senescent cells. This sort of tissue environment is more hospitable to the development of cancer. Cancer risk is far from the only downside of carrying excess visceral fat tissue, of course: one can expect a shorter, less healthy life on all fronts, accompanied with a raised lifetime medical cost.


Obesity is an established risk factor for several cancers. Adult weight gain has been associated with increased cancer risk, but studies on timing and duration of adult weight gain are relatively scarce. We examined the impact of body mass index (BMI) and weight changes over time, as well as the timing and duration of excess weight, on obesity- and non-obesity-related cancers. We pooled health data from six European cohorts and included 221,274 individuals with two or more height and weight measurements during 1972-2014. Several BMI and weight measures were constructed. Cancer cases were identified through linkage with national cancer registries. Hazard ratios (HRs) of cancer were derived from time-dependent Cox-regression models.

During follow-up, 27,881 cancer cases were diagnosed; 9,761 were obesity-related. The HR of all obesity-related cancers increased with increasing BMI at first and last measurement, maximum BMI and longer duration of overweight (men only) and obesity. Participants who were overweight before age 40 years had an HR of obesity-related cancers of 1.16 and 1.15 in men and women, respectively, compared with those who were not overweight. The risk increase was particularly high for endometrial cancer (70%), male renal-cell cancer (58%) and male colon cancer (29%). No positive associations were seen for cancers not regarded as obesity-related. In conclusion, adult weight gain was associated with increased risk of several major cancers. The degree, timing, and duration of overweight and obesity also seemed to be important. Preventing weight gain may reduce the cancer risk.

Link: https://doi.org/10.1093/ije/dyz188

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A Mechanism for Mammalian Cartilage Regrowth is Discovered

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A theme of recent years is the discovery of processes of regrowth that operate in mammalian tissues long thought to be non-regenerative. In this case, researchers have found a mechanism of regeneration that operates in cartilage, albeit not to the degree that would be helpful for recovery from more serious injury or the wear of aging. Still, where a mechanism exists at all, it should be possible to find ways to enhance its operation. This work is interesting for the resemblance that this regenerative process bears to the way in which salamanders regrow lost organ tissue. Finding ways to bring that sort of exceptional regenerative capacity into mammals is the subject of numerous research programs.


Contrary to popular belief, cartilage in human joints can repair itself through a process similar to that used by creatures such as salamanders and zebrafish to regenerate limbs. The mechanism for cartilage repair appears to be more robust in ankle joints and less so in hips. The finding could potentially lead to treatments for osteoarthritis, the most common joint disorder in the world.

Researchers devised a way to determine the age of proteins using internal molecular clocks integral to amino acids, which convert one form to another with predictable regularity. Newly created proteins in tissue have few or no amino acid conversions; older proteins have many. Understanding this process enabled the researchers to use sensitive mass spectrometry to identify when key proteins in human cartilage, including collagens, were young, middle-aged or old. They found that the age of cartilage largely depended on where it resided in the body. Cartilage in ankles is young, it’s middle-aged in the knee and old in the hips. This correlation between the age of human cartilage and its location in the body aligns with how limb repair occurs in certain animals, which more readily regenerate at the furthest tips, including the ends of legs or tails.

The researchers further learned that molecules called microRNA regulate this process. Not surprisingly, these microRNAs are more active in animals that are known for limb, fin or tail repair, including salamanders and zebrafish. These microRNAs are also found in humans – an evolutionary artifact that provides the capability in humans for joint tissue repair. As in animals, microRNA activity varies significantly by its location: it was highest in ankles compared to knees and hips and higher in the top layer of cartilage compared to deeper layers of cartilage.

“We were excited to learn that the regulators of regeneration in the salamander limb appear to also be the controllers of joint tissue repair in the human limb. We believe we could boost these regulators to fully regenerate degenerated cartilage of an arthritic joint. If we can figure out what regulators we are missing compared with salamanders, we might even be able to add the missing components back and develop a way someday to regenerate part or all of an injured human limb. We believe this is a fundamental mechanism of repair that could be applied to many tissues, not just cartilage.”

Link: https://corporate.dukehealth.org/news-listing/humans-have-salamander-ability-regrow-cartilage-joints

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Vitamin C Lowers Mortality in Severe Sepsis

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One of the leading causes of death in American hospitals is something many are still unfamiliar with: septicemia (sepsis or septic shock). Also known as blood poisoning among lay people, sepsis1 is a last-ditch effort by your immune system to fight an infection in your body, which can lead to multiple organ failure and death unless promptly treated. As explained by the National Institute of General Medical Sciences:2

“The body releases immune chemicals into the blood to combat the infection. Those chemicals trigger widespread inflammation, which leads to blood clots and leaky blood vessels. As a result, blood flow is impaired, and that deprives organs of nutrients and oxygen and leads to organ damage.

In severe cases, one or more organs fail. In the worst cases, blood pressure drops, the heart weakens, and the patient spirals toward septic shock. Once this happens, multiple organs — lungs, kidneys, liver — may quickly fail, and the patient can die.”

While viruses, fungi and parasites all have the ability to trigger sepsis, bacterial infections are currently the most common cause. The most common types of infection triggering sepsis are respiratory and urinary tract infections.3 That said, research4 has demonstrated the number of fungal-induced sepsis infections is on the rise.

The problem is that sepsis is often overlooked as many are unfamiliar with its signs and symptoms. It’s also notoriously difficult to treat. A successful outcome relies on early detection and rapid treatment.

Sepsis Is the Costliest Condition Treated in the US

Each year, an estimated 1 million Americans get sepsis5,6 and up to half of them die as a result.7,8,9 According to data10 from two hospital cohorts, 34.7% to 55.9% of American patients who died in hospitals between 2010 and 2012 had sepsis at the time of their death (depending on which inpatient population they were in).

Experts are now calling for recognition11 of sepsis as a distinct cause of death, hoping this will result in better clinical practice guidelines. They also stress the importance of awareness in the community and the emergency room. To this end, September 13 has been designated “World Sepsis Day” to raise awareness.12

Conventional treatment, which is typically focused on high doses of antibiotics that further contribute to antibiotic resistant bacteria, is also a tremendous financial burden. A U.S. government report13,14 published in 2016 found sepsis was the most expensive condition treated in the U.S., racking up $23.7 billion in health care costs each year.

The good news is there’s an inexpensive treatment that has been shown to be very effective against sepsis. The bad news is the number of hospitals that have adopted it as standard of care is still limited.

Vitamin C Concoction — An Inexpensive Cure for Sepsis

In 2017, news emerged about a critical care physician who claimed to have discovered a simple and inexpensive way to treat sepsis using an intravenous (IV) cocktail of vitamin C and thiamine (vitamin B1) in combination with the steroid hydrocortisone.15,16

The precise protocol used was 200 mg of thiamine every 12 hours, 1,500 mg of ascorbic acid every six hours, and 50 mg of hydrocortisone every six hours.17

The doctor in question, Dr. Paul Marik, chief of pulmonary and critical care medicine at Sentara Norfolk General Hospital in East Virginia, published a small retrospective before-after clinical study18,19,20 showing that giving septic patients this simple IV cocktail for two days reduced mortality from 40% percent to 8.5%.

Sentara Norfolk General Hospital, where Marik works, has since made the protocol its standard of care for sepsis, and others are starting to join in. Unfortunately, many hospitals are still dragging their heels, waiting for more clinical trials to be completed.

This despite the fact that the treatment is harmless in and of itself, meaning it won’t make the patient any worse than he or she already is. A 2018 review21 of the available research presents a hypothetical model for why and how the Marik protocol actually works, discussing how each of the three components are known to impact the biological processes involved in sepsis.

As noted in that review,22 reception of the treatment has been mixed, with some critical care leaders embracing it while others aren’t using it at all. What this means is that your ability to receive this potentially life-saving treatment is dependent on the hospital where you end up. 

On the upside, “Enthusiasm for this drug combination in sepsis has grown rapidly” since the release of Marik’s initial study results, and much larger studies are now underway.

One of them is the VICTAS study23 (Vitamin C, Thiamine and Steroids in Sepsis), sponsored by Emory University, which expects to have about 2,000 participants. The projected completion date for this study is October 2021, although preliminary results may become available as early as December 2019.

What to Do if Your Doctor Refuses to Administer This

If your doctor refuses to consider Marik’s protocol offhand, convince him or her to review the recent studies cited here that show this works.24,25,26,27,28,29,30,31,32,33 Simply look up the references in the endnotes to the previous sentence (references 24 through 33) and make copies to take to your doctor.

Alternatively, you can go to PubMed34 directly and type in “vitamin C” and “sepsis” in the search engine and you will get a list of the available research.

These articles are completely free to download. I hope you never need to access them, but if you do, you can print them and use the information to convince your medical team to use these simple life-saving strategies. If they refuse, I would strongly suggest you take control of the situation and find another doctor and/or hospital that will.

Vitamin C Alone May Lower Mortality Risk

Most recently, a study35,36,37,38 led by Dr. Alpha “Berry” Fowler was published in the October 2019 issue of JAMA. The study is not reflective of the Marik protocol per se, as it only used IV vitamin C, but its results are still tantalizing.

Fowler and his team sought to investigate the effectiveness of vitamin C infusion on organ failure scores and biomarkers of inflammation and vascular injury in patients with severe sepsis and acute respiratory failure.

Curiously, while the vitamin C infusion had no detectable influence on these end points, those who received the treatment did have a higher chance of survival, and spent less time in the hospital. As reported by NPR:39

“If you read the study summary, vitamin C didn’t help the patients. But if you dig deep into the paper, you will find that the people who got the treatment were much more likely to survive … The rub comes from the way the study … was designed.”

While vitamin C alone had no impact on organ failure scores and biomarkers of inflammation, when the researchers looked at 46 secondary endpoints, they discovered the mortality rate for the treatment group actually dropped from 46% to 30%. As noted by NPR:40

If death had been the primary endpoint of the study, this result would have been highly significant. The conclusion would strongly support the hypothesis that vitamin C is an effective treatment of sepsis.

But there’s a catch. Since Fowler and his colleagues looked at 46 secondary endpoints, it’s likely that something would randomly pop up as statistically significant. It’s as though they had 46 bites at the apple to find something meaningful …

What patients really care about, of course, is … whether they live or die. Fowler tells NPR that he now rues his decision to select an endpoint that seemed more likely to show a benefit …

Though he’s now bound by the rules of experimental design to downplay the mortality results, he personally feels a sense of success. ‘We’re all whooping and hollering because of what we found,’ he says.”

Fowler’s team also found that, on average, those who received vitamin C had by day 28 spent three fewer days in the intensive care unit than the placebo group (seven days compared to 10). By day 60, the treatment group had also spent seven fewer days in the hospital overall —15 days compared to 22.41

Vitamin C, Thiamine and Steroids Have Synergistic Effects

When asked for comment on Fowler’s study, Marik pointed out vitamin C and corticosteroids have a synergistic effect. In other words, Fowler’s study cannot really be used to judge the effectiveness of vitamin C, thiamine and steroids in combination, as it only used one of the three ingredients.

Vitamin C is well-known for its ability to prevent and treat infectious diseases on its own. Influenza,42 encephalitis and measles43 have all been successfully treated with high-dose vitamin C, and previous research has shown it effectively lowers proinflammatory cytokines and C-reactive protein.44,45,46

To investigate the mechanism of action for vitamin C in sepsis with and without steroids, Marik, in collaboration with John Catravas, Ph.D., a pharmacology researcher at Old Dominion University, and others performed a study47 in which endothelial cells from lung tissue were exposed to lipopolysaccharide — a type of endotoxin found in patients with sepsis — in the absence or presence of ascorbic acid and hydrocortisone.

Interestingly, when either vitamin C or the steroid were administered in isolation, very little improvement in endothelial barrier function occurred. When administered together, however, the infection was successfully eradicated and the cells were restored to normal.

The addition of thiamine is also important. Not only is thiamine required for metabolism of some of the metabolites of vitamin C, thiamine deficiency syndrome (beriberi) has many similarities to sepsis, and thiamine deficiency is relatively common in critically ill patients.48

Studies have also shown thiamine can be helpful for a long list of diseases and disorders, including mitochondrial disorders,49 heart failure,50 delirium,51 thyroid fatigue and Hashimoto’s (a thyroid autoimmune disorder).52 These and other health effects may help explain why thiamine works so well in conjunction with vitamin C and hydrocortisone for sepsis.

Marik told NPR that Fowler’s study does highlight two important things, though. First, that there are no side effects of vitamin C infusion in critically ill patients and, second, a lowered mortality risk. “You can argue about all the statistical nuances, but that’s what the study showed,” Marik told NPR.53

Potential Contraindication

While vitamin C and thiamine administration is incredibly safe, it may be contraindicated if you happen to be glucose-6-phosphate dehydrogenase (G6PD) deficient, which is a genetic disorder.54 G6PD is an enzyme your red blood cells need to maintain membrane integrity.

High-dose IV vitamin C is a strong prooxidant, and giving a prooxidant to a G6PD-deficient individual can cause their red blood cells to rupture, which could have disastrous consequences.

Fortunately, G6PC deficiency is relatively uncommon, and can be tested for. People of Mediterranean and African descent are at greater risk of being G6PC deficient. Worldwide, G6PD deficiency is thought to affect 400 million individuals, and in the U.S. an estimated 1 in 10 African-American males have it.55

Know the Signs and Symptoms of Sepsis

One of the most important steps you can take to protect your health is to recognize the symptoms of sepsis and seek immediate medical attention if you suspect it.

It is important not to make a diagnosis at home. Instead communicate your concerns with a medical professional so that proper testing and treatment can be implemented. Common signs and symptoms of sepsis include the following.56,57,58 Many of these symptoms may be confused with a bad cold or the flu. However, they tend to develop much more rapidly than you would normally expect.

A high fever with chills and shivering

Rapid heartbeat (tachycardia)

Rapid breathing (tachypnea)

Unusual level of sweating (diaphoresis)

Dizziness

Confusion or disorientation

Slurred speech

Diarrhea

Difficulty breathing, shortness of breath

Severe muscle pain

Low urine output

Cold and clammy skin

Skin rash

Nausea and/or vomiting

The Sepsis Alliance recommends using the acronym TIME to remember some of the more common symptoms:59

  • T — Temperature higher or lower than normal?
  • I — Have you now or recently had any signs of an infection?
  • M — Are there any changes in mental status, such as confusion or excessive sleepiness?
  • E — Are you experiencing any extreme pain or illness; do you have a “feeling you may die?”

Post-Sepsis Syndrome

While some will recover fully from sepsis, for many the problems do not end at discharge from the hospital. Survivors may suffer physical, psychological and/or neurological consequences for the rest of their lives. For some survivors, their immune function can remain depressed for as long as a year after their recovery, resulting in frequently recurring infections.

The combination of symptoms is called post-sepsis syndrome and usually last between six and 18 months. Symptoms of post sepsis syndrome may include:60,61

Lethargy (excessive tiredness)

Changes in peripheral sensation

Repeated infections at the original site or a new infection

Poor mobility

Muscle weakness

Shortness of breath

Chest pains

Swollen limbs

Joint and muscle pains

Depression, mood swings, anxiety or sadness

Hair loss

Dry flaking skin and nails

Taste changes

Poor appetite

Changes in vision

Difficulty swallowing

Reduced kidney function

Feeling cold

Excessive sweating

Post-traumatic stress disorder

Flashbacks and nightmares

Poor concentration and clouded thinking

Insomnia

Short-term memory loss

There is no specific treatment for post-sepsis syndrome, but most get better over time. The U.K. Sepsis Trust62 recommends managing individual symptoms and supporting optimal health as you’re recovering.

Not all medical professionals are aware of post-sepsis syndrome, so it may be helpful to talk about your symptoms and ask for a referral to someone who may help manage your mental, physical and emotional challenges.

How to Reduce Your Risk of Sepsis

Again, part of what makes sepsis so deadly is people typically do not suspect it, and the longer you wait to treat it, the deadlier it gets.63 If you develop an infection, stay alert to symptoms of sepsis and seek immediate medical attention if they appear. Even health care workers can miss the signs and delay treatment.

While health care workers have a responsibility to prevent infections that could potentially turn septic and to educate patients about warning signs of sepsis, you can lower your own risk by:

Promptly treating urinary tract infections (UTIs) — UTIs are the second most common type of infection,64 and one-quarter of sepsis cases are related to UTIs.65

Conventional treatment typically involves antibiotics, but research66,67 shows that UTIs caused by E. coli — which comprise68 90% of all UTIs — can be successfully treated with D-Mannose, a naturally occurring sugar that’s closely related to glucose. To learn more, see “D-Mannose for UTI prevention validated in a clinical trial.”

Properly cleaning skin wounds — About 1 in 10 sepsis cases are due to skin infections, so always take the time to properly clean and care for wounds and scrapes. Wash the wound with mild soap and water to clean out dirt and debris, then cover with a sterile bandage. Diabetics should follow good foot care to avoid dangerous foot infections.

Caring for any chronic illness affecting your risk of sepsis — Research has found illnesses that increase your risk may include chronic lung disease, chronic kidney disease, diabetes, stroke and cardiovascular disease.69

Avoiding nail biting — One study found 46.9% of the participants were nail biters.70 Exposure of the delicate skin underneath the nail, transferred from your mouth or acquired from the environment, increases your risk of infection.

Avoiding infections in hospitals — When visiting a health care facility, be sure to wash your own hands, and remind doctors and nurses to wash theirs (and/or change gloves) before touching you or any equipment being used on you.

If you have to undergo a colonoscopy or other testing using a flexible medical scope, remember to call and ask how they clean their scopes and what kind of cleaning solution they use.

If the answer is glutaraldehyde (brand name Cidex), find another hospital or clinic — one that uses peracetic acid. This preliminary legwork will significantly decrease your risk of contracting an infection from a contaminated scope.

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Lack of Sleep and Chronic Disease Are a Risky Combo

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While sleep is still a largely neglected area of health, research shows that without proper sleep — both in terms of time and quality — every aspect of your health will be adversely impacted. Many important things happen during sleep, and only during sleep.

For example, sleep is required for the maintenance of metabolic homeostasis in and the removal of toxic waste from your brain, as well as the maintenance of biological homeostasis in your body. Without proper sleep, you leave yourself wide-open to chronic illness of all kinds, including diabetes,1 heart disease,2 neurodegeneration3 and cancer.4

According to recent research, lack of sleep when you’re already struggling with a chronic health issue could be a downright deadly prescription. As reported by CNN Health:5

“If you’re a middle-aged adult with high blood pressure, Type 2 diabetes or existing heart disease and you typically sleep less than six hours each night, you could be setting yourself up for cancer or an early death from heart disease.”

Lack of Sleep Makes Chronic Health Problems Extra Risky

The study5,7,8 CNN is referring to was published in the October 2019 issue of the Journal of the American Heart Association (JAHA). In it, researchers sought to determine whether short sleep duration would increase the risk of death associated with cardiometabolic risk factors and cardiovascular and cerebrovascular diseases.

Data from 1,654 adults from the Penn State Adult Cohort were evaluated. Using Cox proportional hazard models, the adjusted hazard ratio for all-cause mortality among those who slept less than six hours and had cardiometabolic risk factors (high blood pressure, elevated glucose or Type 2 diabetes) was 2.14 times higher than those who regularly slept six hours or more.

They also had a 1.83 times higher risk of dying from cardiovascular or cerebrovascular diseases. Among those with a diagnosis of heart disease or stroke, sleeping less than six hours a night increased their all-cause mortality risk by 3.17 times. Interestingly, it also increased their risk of dying from cancer, specifically, by 2.92 times.

All of these associations were found to be independent of age, sex, ethnicity, obesity, smoking and other health conditions that might influence the results. Conversely, sleeping less than six hours did not increase the risk of death in those that did not have cardiometabolic risk factors or a cardiovascular or cerebrovascular disease diagnosis.

Likewise, those with cardiometabolic risk factors or a cardiovascular or cerebrovascular disease diagnosis who slept six hours or more were not at increased risk for death either. It was specifically the combination of chronic health problems and short sleep duration that increased the risk of death, including cancer mortality.

Sleep Duration Plays a Role in Mortality Prognosis

As noted by the authors:9

“Our novel findings show that objective short sleep duration increases the mortality risk of middle‐aged adults with CMRs [cardiometabolic risk factors] and those who have already developed CBVD [cardiovascular and cerebrovascular diseases].

Middle‐aged adults with CMR who slept <6 hours were at a high risk of dying from CBVD, whereas middle‐aged adults with CBVD who slept <6 hours were at a high risk of dying from cancer …

If these findings are replicated in other large cohorts with objective sleep measures, short sleep duration should be included in the prediction of the mortality prognosis of middle‐aged adults with CMR or CBVD.

The primary finding of the current study indicated that there was an ≈2‐fold risk for all‐cause, CBVD, and non‐CBVD mortality in participants who had CMRs at baseline and demonstrated short sleep duration in the sleep laboratory.

Individuals who had CMRs and normal sleep duration at baseline, on the other hand, did not show a significantly increased risk on any of the mortality outcomes. This finding suggests that obtaining an adequate amount of sleep may minimize the adverse effect of CMRs on multiple mortality outcomes.

For instance, participants with both CMRs and short sleep at baseline showed an 83% higher risk of dying from CBVD, whereas their CMR counterparts with normal sleep duration had a modest 35% nonsignificant higher risk of CBVD mortality …

In conclusion, objective short sleep duration is an effect modifier of the mortality risk associated with CMR or CBVD. More important, our data suggest that short sleep may operate through different mechanisms on CBVD versus cancer mortality.”

Lack of Sleep Raises Your Risk for Heart Disease

That short sleep duration and/or poor sleep quality raises your risk of heart disease and cancer has been repeatedly demonstrated. For example, a study10 published in the October 2018 issue of Sleep Health found poor sleep excessively ages your heart, which in turn raises your risk of developing heart disease.

As explained by lead author Quanhe Yang, senior scientist in the Division for Heart Disease and Stroke Prevention of the U.S. Centers for Disease Control and Prevention:11

“The difference between a person’s estimated heart age and his or her chronological age is ‘excess heart age’ …

For example, if a 40-year-old man has a heart age of 44 years based on his cardiovascular risk profile — the personal risk of having a heart disease — then his excess heart age is 4 years. In effect, his heart is four years older than it should be, for a typical man his age. The concept of heart age helps to simplify risk communication.”

In this study, people who regularly slept five hours or less had hearts that were biologically 5.1 years older than their chronological age, while those who got seven hours of sleep each night had hearts showing signs of being biologically 3.7 years older than their chronological age.

Interestingly, the association between sleep and excess heart age was not linear. Those getting seven hours of sleep fared the best. At eight and nine hours, excess heart age started rising again, hitting 4.5 at eight hours and 4.1 at nine hours.

Sleep Quality Also Plays a Role in Heart Disease Risk

Another 2018 study12 found that even if you sleep a healthy number of hours, the quality of that sleep can have a significant impact on your risk for high blood pressure and vascular inflammation associated with heart disease.

Women who had mild sleep disturbance such as taking longer to fall asleep or waking up one or more times during the night were far more likely to have high blood pressure than those who fell asleep quickly and slept soundly throughout the night. According to the researchers:13

“Systolic blood pressure was associated directly with poor sleep quality, and diastolic blood pressure … Poor sleep quality was associated with endothelial nuclear factor kappa B activation. Insomnia and longer sleep onset latency were also associated with endothelial nuclear factor kappa B activation …

These findings provide direct evidence that common but frequently neglected sleep disturbances such as poor sleep quality and insomnia are associated with increased blood pressure and vascular inflammation even in the absence of inadequate sleep duration in women.”

Sleep Influences Your Cancer Risk

The influence of sleep is also seen in cancer. As noted in a 2009 study14 in Sleep Medicine Reviews:

“The pineal hormone melatonin is involved in the circadian regulation and facilitation of sleep, the inhibition of cancer development and growth, and the enhancement of immune function.

Individuals, such as night shift workers, who are exposed to light at night on a regular basis experience biological rhythm (i.e., circadian) disruption including circadian phase shifts, nocturnal melatonin suppression, and sleep disturbances.

Additionally, these individuals are not only immune suppressed, but they are also at an increased risk of developing a number of different types of cancer.”

As explained in this paper, while melatonin plays an important role, there’s a reciprocal interaction between sleep and your immune system that is independent of melatonin as well. When your sleep cycle is disrupted, your immune function can be suppressed, allowing cancer-stimulating cytokines to proliferate and dominate. According to the authors:

“The mutual reinforcement of interacting circadian rhythms of melatonin production, the sleep/wake cycle and immune function may indicate a new role for undisturbed, high quality sleep, and perhaps even more importantly, uninterrupted darkness, as a previously unappreciated endogenous mechanism of cancer prevention.”

Similarly, research15 published in 2012 found sleep-disordered breathing or sleep apnea increases your risk of dying from cancer. Those with moderate sleep apnea were twice as likely to die from cancer, compared to those able to breathe normally during sleep. Those with severe sleep apnea had a 4.8 times higher cancer mortality.

Melatonin Is a Powerful Cancer Preventive

While it may not be the sole mechanism, decreased levels of melatonin due to lack of sleep certainly appears to play a key role in cancer formation. In one study, 16 postmenopausal women who regularly slept nine hours or more had a 33% lower risk of breast cancer than those who slept six hours or less.

This inverse association was strongest in lean women. The researchers confirmed that melatonin levels rose in tandem with reported hours of sleep. On average, melatonin levels in those who slept at least nine hours were 42% higher than in those who got six hours or less.

Importantly, melatonin both inhibits the proliferation of cancer cells and triggers cancer cell apoptosis17 (self-destruction). It also interferes with the new blood supply tumors required for their rapid growth (angiogenesis).18

A paper19 in the International Journal of Experimental Pathology also points out that melatonin modulates not only the production of blood cells and platelets in your bone marrow (haemopoiesis) but also the production of immune cells. It also plays a role in the function of those immune cells. As explained in the introduction of this paper:

“Physiologically, melatonin is associated with T‐helper 1 (Th1) cytokines, and its administration favors Th1 priming. In both normal and leukemic mice, melatonin administration results in quantitative and functional enhancement of natural killer (NK) cells, whose role is to mediate defenses against virus‐infected and cancer cells.

Melatonin appears to regulate cell dynamics, including the proliferative and maturational stages of virtually all hematopoietic and immune cells lineages involved in host defense — not only NK cells but also T and B lymphocytes, granulocytes and monocytes — in both bone marrow and tissues.

In particular, melatonin is a powerful antiapoptotic signal promoting the survival of normal granulocytes and B lymphocytes. In mice bearing mid‐stage leukemia, daily administration of melatonin results in a survival index of 30–40% vs. 0% in untreated mice.

Thus, melatonin seems to have a fundamental role as a system regulator in hematopoiesis and immuno‐enhancement, appears to be closely involved in several fundamental aspects of host defense and has the potential to be useful as an adjuvant tumor immunotherapeutic agent.”

General Sleep Guidelines

Considering the importance of sleep for preventing the two top killers in the U.S. (heart disease and cancer), just how much sleep do you need to reap protective benefits?

According to a scientific review of more than 300 studies published between 2004 and 2014, a panel of experts came up with the following recommendations. Keep in mind that if you’re sick, injured or pregnant, you may need a bit more than normal.

Age Group Hours of sleep needed for health

Newborns (0 to 3 months)

14 to 17 hours

Infants (4 to 11 months)

12 to 15 hours

Toddlers (1 to 2 years)

11 to 14 hours

Preschoolers (3 to 5)

10 to 13 hours

School-age children (6 to 13)

9 to 11 hours

Teenagers (14 to 17)

8 to 10 hours

Adults (18 to 64)

7 to 9 hours

Seniors (65 and older)

7 to 8 hours

Set a Nightly Alarm to Help You Get Enough Sleep

There’s simply no doubt that sleep needs to be a priority in your life if you intend to live a long and healthy life. For many, this means forgoing night-owl tendencies and getting to bed at a reasonable time.

If you need to be up at 6 a.m., you need a lights-out deadline of 9:30 or 10 p.m., depending on how quickly you tend to fall asleep. If you find it difficult to get to bed on time, consider setting a bedtime alarm to remind you that it’s time to shut everything down and get ready for sleep.

As for how to improve your sleep if you’re having trouble falling or staying asleep, see my “Top 33 Tips to Optimize Your Sleep Routine.”

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Increased Insulin Sensitivity is Not Required for Extension of Healthy Life Span in Mice via Calorie Restriction

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The biochemistry surrounding insulin and insulin signaling is very well studied in the context of aging. A number of ways to slow aging in laboratory species involve directly manipulating these signaling pathways. Calorie restriction, like a number of other methods of slowing aging, improves insulin sensitivity, and the consensus in the research community has been that some fraction of the benefits to health and longevity that result from a restricted calorie intake are derived from this change to insulin metabolism. Today’s open access paper provides evidence to suggest, surprisingly, that this is not in fact the case. It is possible to block this part of the calorie restriction response, and the effect on health and longevity is much the same.

What, then, are the mechanisms by which calorie restriction produces extension of life span in short-lived species? The evidence to date points towards upregulation of autophagy. Autophagy is the name given to a collection of processes responsible for recycling damaged or unwanted cellular structures and protein machinery. Many methods of slowing aging in laboratory species prominently feature increased autophagy; in principle, cells that are better maintained will experience fewer issues and this results in better tissue function and a slower decline into age-related degeneration. Certainly, it is the case that when autophagy is disabled, then calorie restriction no longer acts to extend life.

Calorie-Restriction-Induced Insulin Sensitivity Is Mediated by Adipose mTORC2 and Not Required for Lifespan Extension


Calorie restriction (CR), a dietary regimen in which calories are reduced without causing malnutrition, extends the lifespan of many diverse species and is the gold standard for interventions that promote the health and longevity of mammals. Importantly, CR extends not only longevity but also healthspan. There has therefore been great interest in identifying the physiological and molecular mechanisms by which CR promotes health and longevity.

In mammals fed a CR diet, one of the most striking and broadly conserved effects is improved sensitivity to insulin. Many dietary and pharmaceutical interventions that extend mammalian lifespan and healthspan likewise promote insulin sensitivity, while conversely, there is a well-known association of insulin resistance with diabetes and poor health. Given the central role of the insulin signaling pathway in the lifespan of worms, flies, and mammals, improved insulin sensitivity has been proposed as an essential mechanism by which a CR diet extends mammalian lifespan. While the effects of CR are systemic, some of its most prominent effects are on adipose tissue; CR reduces adiposity in mammals, mobilizing fat stores in white adipose tissue (WAT) while also activating WAT lipogenesis, which is associated with improved systemic insulin sensitivity and metabolic health.

Despite the strong correlative evidence that CR promotes health and longevity through improved insulin sensitivity, there is clear evidence that insulin sensitivity may not necessarily be essential for healthy aging. Several genetically modified mouse models in which insulin resistance has been induced in one or more tissues have extended lifespan, while mice treated with rapamycin, an inhibitor of the mTOR (mechanistic target of rapamycin) protein kinase that extends lifespan, develop insulin resistance in multiple tissues.

Over the last decade, a critical role for mTOR complex 2 (mTORC2) in the control of organismal metabolism has become apparent. In contrast to the well-known mTOR complex 1 (mTORC1), which functions as a key integrator of many different environmental and hormonal cues, mTORC2 functions primarily as an effector of phosphatidylinositol 3-kinase (PI3K) signaling, contributing to the downstream activation of many kinases, including AKT, by insulin. Deletion of Rictor, which encodes an essential protein component of mTORC2, results in insulin resistance in tissues, including liver, adipose tissue, and skeletal muscle. The organismal consequences of inactivating adipose mTORC2 have been unclear.

While an important role for CR-induced insulin sensitivity in the health and survival benefits of CR has long been assumed, the contribution of improved insulin sensitivity to the benefits of CR has not been directly examined. Here, we have tested the role of CR-induced insulin sensitivity on the metabolic health, frailty, and longevity of mice by placing mice lacking adipose mTORC2 signaling (AQ-RKO) and their wild-type littermates on either ad libitum or CR diets. Critically, the insulin sensitivity of AQ-RKO mice does not improve on a CR diet, enabling us to discern the role of CR-induced insulin sensitivity in CR-induced phenotypes. Although the WAT of AQ-RKO mice has a blunted metabolic response to CR and female AQ-RKO mice fed an ad libitum diet have a slightly reduced lifespan, we find that AQ-RKO mice of both sexes fed a CR diet have increased fitness and extended lifespan. We conclude that the CR-induced increase in insulin sensitivity is dispensable for the effects of CR on fitness and longevity.

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Why Does Reduced Grip Strength Correlate with Chronic Lung Disease in Aging?

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In this open access paper, researchers speculate on the common mechanisms underlying the correlation between reduced grip strength and chronic lung disease in old age. The many, complex, and diverse manifestations of aging emerge from a much smaller, simpler set of root causes. Simple forms of damage applied to a very complex system necessarily produce very complex outcomes. Nonetheless, the incidence of many of those outcomes, even when very different from one another, will correlate because they depend to a sizable degree on the same forms of underlying damage.


The term “sarcopenia” was first introduced to describe the progressive age-related loss of muscle mass and is correlated with poor health-related quality of life. In this context, the handgrip dynamometer (HGD) is a useful tool to evaluate muscle strength because it provides simple, fast, reliable, and standardized measurements of total muscle strength. In addition, handgrip strength (HGS) is considered an important measure to diagnose dynapenia because low HGS is a robust predictor of low muscle mass and a clinical marker of poor physical performance.

In the respiratory system, the incidence of chronic lung diseases (CLDs) is comparatively higher in individuals aged 65 and older. HGS is an indicator of overall physical capacity. It is not limited to assessing the upper limbs and is a good predictor of morbidity and mortality, indicating that the HGD is a potentially useful instrument for evaluating different populations with different respiratory conditions. Despite these advantages, HGS is rarely used as a functional measure in patients with respiratory diseases, perhaps because it is erroneously considered a part of a complex battery of functional tests.

Current evidence indicates the presence of different phenomena linking lower muscle mass and function with the occurrence of CLDs in this population. Chronic systemic inflammation is related to nontransmissible CLDs in the elderly, and this inflammatory status may be one of the main links to reduced HGS. In addition to systemic inflammation, other contributors that appear to be important are the chronic effects of hypoxemia due to CLDs, physical inactivity, respiratory and peripheral myopathy, malnutrition, and the use of corticosteroids, which is common in many CLDs. Sarcopenic obesity is increasingly diagnosed in different clinical conditions and may be an important link between decreased HGS and adiposity in CLDs. Reduced HGS in CLDs should be considered a systemic phenomenon requiring a holistic approach to restore physical reconditioning and nutritional status. Therefore, early targeted interventions should be developed in patients with CLDs to delay muscle strength decline and prevent functional limitations and disabilities.

Link: https://doi.org/10.14336/AD.2018.1226

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Business Analysts Start to Pay Attention to the Longevity Industry

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Larger business analysis concerns are starting to notice that the longevity industry exists. I point out this press release not because the contents are all that interesting or useful – it is very much business as usual in the white paper production community, and the people creating these materials typically have a poor understanding of the biology and the biotechnology – but rather as an indication of progress towards a broader appreciation of the potential to treat aging as a medical condition. Slowly, the eyes of the world are opened.


The global longevity and anti-senescence market will witness rapid growth over the forecast period (2018-2023) owing to an increasing emphasis on stem cell research and increasing demand for cell-based assays in research and development. An increasing geriatric population across the globe and rising awareness of antiaging products among generation Y and later generations are the major factors expected to promote the growth of a global longevity and anti-senescence market. Factors such as a surging level of disposable income and increasing advancements in anti-senescence technologies are also providing traction to the global longevity and anti-senescence market growth over the forecast period (2018-2023).

Senolytics, placenta stem cells, and blood transfusions are some of the hot technologies picking up pace in the longevity and anti-anti-senescence market. Companies and start-ups across the globe such as Unity Biotechnology, Human Longevity Inc., Calico Life Sciences, Acorda Therapeutics, etc. are working extensively in this field for the extension of human longevity by focusing on the study of genomics, microbiome, bioinformatics, and stem cell therapies, etc. Senolytic drug therapy held the largest market revenue share in 2017. The fastest growth of the gene therapy segment is due to the large investments in genomics.

The scope of this report is broad and covers various therapies currently under trials in the global longevity and anti-senescence therapy market. The market estimation has been performed with consideration for revenue generation in the forecast years 2018-2023 after the expected availability of products in the market by 2023. The global longevity and anti-senescence therapy market has been segmented by the following therapies: senolytic drug therapy, gene therapy, immunotherapy, and other therapies which includes stem cell-based therapies, etc. Forecasts from 2028 to 2023 are given for each therapy and application, with estimated values derived from the expected revenue generation in the first year of launch.

Link: https://www.businesswire.com/news/home/20191016005347/en/Global-Longevity-Anti-Senescence-Therapy-Market-Review-2017-2018

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Vitamin A Can Save Your Skin

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Skin cancer is the most common form of cancer found in the U.S., and the most common of those are basal and squamous cell cancers.1 Although death from these types is uncommon,2,3 the consequences of treatment may be disfiguring.

Despite recommendations for people to stay out of the sun and use sunscreen, current estimates4 are that the lifetime risk for skin cancer is 20% for Americans. Approximately 9,500 skin cancers are diagnosed every day. But, sensible sun exposure, while taking care to avoid getting burned, is one of the best ways to optimize your vitamin D level.

Researchers estimate 85% of children living in urban areas, and half of all adults and the elderly suffer from vitamin D deficiency.5 This is in spite of the fact that Americans are used to eating fortified foods.

Vitamin D deficiencies may be due in part from recommendations by dermatologists to avoid sun exposure6,7 as they attempt to curb the rising number who suffer from skin cancer. As researchers have found,8 it is UVA rays that trigger cell damage that leads to skin cancer. You can be exposed to UVA rays both inside and outdoors.

Nonmelanoma types of skin cancer, including squamous cell and basal cell, affect more than 3 million people in the U.S. each year, demonstrating the need for more effective preventive strategies to be used.

Study Shows Vitamin A Reduces Skin Cancer

In a recent study9 published in the Journal of the American Medical Association it was reported that researchers sought to find out whether vitamin A was associated with a reduction in the incidence of squamous cell skin cancer. The team enrolled 123,570 men and women and followed them for more than 26 years, evaluating their dietary intake of vitamin A.

Any incidence of skin cancer was confirmed by pathology reports. The researchers believe the data suggest increasing your dietary intake of vitamin A reduces your risk of squamous cell carcinoma. This team, from Brown University, was led by Eunyoung Cho, who commented on the results:10

“Our study provides another reason to eat lots of fruits and vegetables as part of a healthy diet. Skin cancer, including squamous cell carcinoma, is hard to prevent, but this study suggests that eating a healthy diet rich in vitamin A may be a way to reduce your risk, in addition to wearing sunscreen and reducing sun exposure.”

The researchers accounted for factors such as hair color, number of severe burns participants may have experienced and family history.11 Participants were not asked about their exposure to the sun during the middle of the day.

Participants who ate the highest amount of vitamin A consumed the equivalent of two large carrots each day. Those who ate the least amount had the equivalent of one small carrot, which the researchers note is well within the U.S. recommended dietary allowance.

Data indicate that those who ate the highest amount of vitamin A during the day had a 17% reduction in the potential for skin cancer, as compared to those who consumed the lowest. Evaluation of dietary intake also showed vitamin A from the group eating the most came from fruits and vegetables rather than animal-based foods or supplements.12

Vitamin A plays an important role in regulating cell growth and differentiation. Thus, it participates in mitigation of the development of cancer and modulates age-related macular degeneration and vision loss.13 Although frank deficiency is rare in the U.S., it is not uncommon in developing countries where people have limited access to vitamin A rich foods.14

Vitamin B3 and Vitamin D May Offer Additional Protection

Two other vitamins important in the prevention of skin cancer include vitamin B3 (nicotinamide) and vitamin D, metabolized in your skin during exposure to the sun. In the third phase of an Australian study15 evaluating the effect of vitamin B3 in individuals with nonmelanoma skin cancers, researchers enrolled participants who had at least two nonmelanoma skin cancers in the past five years.

They assigned participants to receive either 500 mg of vitamin B3 twice a day or a placebo over the course of the following 12 months. The data showed no side effects with the placebo or vitamin B3. In the 12-month study, those taking vitamin B3 experienced a 23% lower rate of new skin cancers. However, once the vitamin B3 was discontinued, there was no continued benefit.

Sunburns, especially when you’re young, are associated with an increased risk of melanoma. Yet, melanomas often appear in areas of the body rarely exposed to the sun. Also noteworthy, though, is that a lack of exposure to the sun reduces the amount of vitamin D your body produces, which is protective against melanoma. In a study published in the Lancet, researchers wrote:16

“Paradoxically, outdoor workers have a decreased risk of melanoma compared with indoor workers, suggesting that chronic sunlight exposure can have a protective effect. Further, some melanomas form on sun-exposed regions; others do not. Although some melanomas arise from pre-existing melanocytic naevi (moles), many arise de novo.”

Evidence suggests it is wise to get sensible unprotected sun exposure on a large amount of skin to a point just short of your skin turning pink. Then, cover up with a thin layer of clothing to protect your skin from burns. If you’re outdoors for long periods of time, wear a wide-brimmed hat since the skin on your face is more prone to damage but does not add much to the manufacture of vitamin D.

Avoiding the sun may be dangerous to your health as a Swedish study17 demonstrated. The researchers looked at sun avoidance as a risk factor for all-cause mortality in 29,518 women over a 20-year period. They concluded that avoiding sun exposure is a risk for all-cause mortality and restricting exposure in countries with low solar intensity may be harmful.

Do Avoid Sunburns and Chemical Sunscreens

The American Academy of Dermatology18 recommends staying out of tanning beds and protecting your skin by “seeking shade, wearing protective clothing and using a broad-spectrum, water-resistant sunscreen with an SPF of 30 or higher.”

As you consider the recommendations for sun exposure, it’s important to remember that avoiding it altogether places you at greater risk for several internal cancers, which I discussed in my past article, “Vitamins That Reduce Your Risk of Skin Cancer.”

It is also important to avoid sunburn, since overexposure can result in cell damage and raise your risk of skin cancer. If you plan on spending a day at the beach or engaging in outdoor activities for long hours, you’ll need some form of sun protection. Light clothing is the ideal choice, but most people still opt for sunscreen.

Unfortunately, many sunscreen products contain toxic ingredients. The 2018 Sunscreen Buying Guide from Consumer Reports19 notes that many products did not provide the level of UVB protection printed on the label.

As a result, you may be exposed to toxic chemicals and end up getting sunburned anyway. For a more thorough discussion of the toxins found in, and the effectiveness of, sunscreens see my past articles:

Use Your Diet to Increase Vitamin A

Increasing your food sources of vitamin A is the most effective means of achieving optimal levels. Foods high in vitamin A include sweet potatoes, spinach, carrots, cantaloupe and mangoes.20 Other vegetables that offer this same benefit include kale, mustard greens, collard greens and turnip greens.21

Vitamin A is a group of nutrients that falls into two different categories: retinoids found in animal foods and carotenoids found in plant foods. The two are chemically different and provide different health benefits, but both are necessary for optimal health.

Most carotenoids function as anti-inflammatory and antioxidant agents while retinoids are important for red blood cell production. They’re especially necessary during pregnancy and in helping the body resist infections.

Choose Astaxanthin to Protect Yourself From the Inside Out

Astaxanthin is a part of the carotenoid family and may be one of the most potent antioxidants. It’s produced by microalgae as a protective mechanism to shield it from ultraviolet light and other environmental stressors.22 It has a unique molecular structure that helps protect your skin from the inside out.

Specifically, it helps protect against UV-induced cell death. Unlike topical sunblock, it does not block UV rays, so it doesn’t prevent the conversion of vitamin D in your skin. In addition, it increases your skin’s elasticity and reduces the appearance of fine lines and wrinkles.

Astaxanthin is a powerful antioxidant exhibiting neuroprotective effects. It benefits your cardiovascular system and also protects your vision. It can help reduce post-exercise recovery time and soreness and is being considered by NASA to offset the damage from radiation exposure in space. Read more about the rising number of benefits researchers have discovered that are associated with astaxanthin in these articles:

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