Amyloid-β Aggregation Accelerates Age-Related Activation of Microglia

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This open access paper is illustrative of present work on the role of microglial dysfunction and chronic inflammation in Alzheimer’s disease. The central nervous system immune cells called microglia become inappropriately inflammatory with age. A new consensus on Alzheimer’s disease is that initial amyloid-β accumulation causes far greater than usual chronic disarray and inflammatory signaling in the supporting cells of the brain, such as microglia, astrocytes, and oligodendrocytes. This in turn leads to the much more damaging tau aggregation and consequent damage and death of neurons.


Alzheimer’s disease (AD) is characterized by typical biochemical lesions (β-amyloid peptide [Aβ] plaques and tau tangles) accompanied by extensive cellular changes (neuronal dystrophic alterations, neuronal cell loss, astrogliosis, and microgliosis). Rare mutations in amyloid precursor protein (APP), presenilin 1 and presenilin 2 trigger Aβ plaque accumulation and are sufficient to induce the full biochemical and morphological signature of AD. While this clearly indicates a major role for Aβ in AD pathology even in these genetic forms, a decades-long asymptomatic phase is present. Thus, in addition to Aβ plaques, other pathological processes, either in response to or in parallel to Aβ accumulation, need activation to cause neurodegenerative disease.

The search for the genetic risk determinants in sporadic AD has highlighted the central role of non-neuronal genes in pathways that do not appear directly related to Aβ metabolism. Most of the genes associated with the ∼40 loci identified by genome-wide association (GWA) analysis or by rare variant sequencing studies are expressed in glial cells. Moreover, analysis of available single-cell transcriptome datasets for human brain cells reported an association between AD GWA signals and microglia as well as astrocytes. Analysis of regulatory networks of genes differentially expressed in AD patients indicates that immune- and microglia-specific gene modules are key contributors to AD pathology.

Thus, genetic and molecular evidence suggest that Aβ accumulation is the trigger of a series of pathogenic processes in which microglia play a central role. No consistent hypothesis, however, links the causality implied by the mutations in the amyloid pathway genes to the genetic risk linking sporadic AD to inflammatory pathways. One possible resolution is that amyloid pathology acts only as a trigger in sporadic AD; i.e., Aβ accumulation is necessary but insufficient to cause full-blown disease. The cellular response, determined by the genetic makeup of the patients, tilts the table from a rather benign Aβ proteopathy to the severe neurodegeneration with inflammation and tau pathology that characterizes AD. In this regard, further understanding of the microglia response to amyloid pathology and the role of risk factors for AD in this response is key.

Here, we set out to address in a systematic way the question of how microglia respond over time, in cortex and hippocampus, to progressive Aβ deposition and whether this is affected by the three major risk factors for AD, i.e., age, sex, and genetics. We use an App knockin mouse model, which displays progressive amyloidosis and microgliosis. We show that the microglial responses to Aβ pathology are complex but, surprisingly, largely reproducible cell states that are also appearing during normal aging, albeit slower and quantitatively more limited. Moreover, we show that microglia in female mice tend to react earlier and in a more pronounced way than microglia in male mice, particularly in older mice. Interestingly, the major response of microglia to amyloid pathology is enriched for AD risk genes, with Apoe expression, in particular, becoming highly upregulated. This is partially confirmed in human tissue.

Link: https://doi.org/10.1016/j.celrep.2019.03.099

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Repair Biotechnologies Raises a $2.15M Seed Round to Fight Age-Related Diseases

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As many of you know, Bill Cherman and I founded Repair Biotechnologies in 2018 with the intent of developing promising lines of rejuvenation research into clinical therapies. There are many opportunities given the present state of the science and far too few people working on them. This remains true even as large amounts of venture funding are entering the space; our field needs more entrepreneurs. I’m pleased to note that we’re making progress in our pipeline at Repair Biotechnologies, and have recently closed a seed round from notable investors in order to power us through to the next phase of our work.

What does the Repair Biotechnologies team work on? When we initially set out, after a survey of the field, we settled upon regeneration of the thymus via FOXN1 upregulation as the lowest of low-hanging fruit, a project with good evidence in the literature and the potential of a sizable upside to health in later life when realized. The thymus atrophies with age, and this is a major factor in the age-related decline of the immune system, as the thymus is where T cells mature. Reductions in the supply of new T cells eventually leads to an immune system packed with malfunctioning, senescent, and overspecialized cells that are incapable of defending effectively against pathogens and errant cells.

A little later we picked up development of a fascinating line of research relating to the vulnerability of macrophages to cholesterol. The pathologies of atherosclerosis are caused when macrophage cells become ineffective at clearing out cholesterol from blood vessel walls. They are overwhelmed by oxidized cholesterol in particular, but too much cholesterol in general will also do the trick. Macrophages become inflammatory or senescent, and die, adding their debris to a growing fatty plaque that will eventually rupture or block the blood vessel. By giving macrophages the ability to degrade cholesterol, we can in principle reverse atherosclerosis by making macrophages invulnerable to the cause of the condition. This is, we believe, a much better approach that that of trying to reduce cholesterol in the bloodstream.

Repair Biotechnologies Raises $2.15M Seed Round to Develop Drugs for Age-Related Diseases


Repair Biotechnologies, Inc. announced today $2.15 million in seed venture funding, to accelerate the preclinical development of its pipeline of drugs targeting thymus regeneration, cancer, and atherosclerosis. The $2.15 million in funding was led by Jim Mellon, the billionaire investor and chairman of Juvenescence Ltd. Also participating in the round are Emerging Longevity Ventures, Thynk Capital, and SENS Research Foundation.

“We are committed to developing treatments for the root causes of aging and its associated diseases through the damage repair approach,” said Reason, co-founder and CEO. “With this funding round, we will be able to further develop our therapies and validate them in animal models, bringing them closer to the clinic and patients.”

The thymus gland is vital to the adaptive immune system, but with age, the thymus shrinks, leading to a decreased immune cell production and a compromised immune system. Repair Biotechnologies is developing a therapy with the aim of reverting this atrophy of the thymus, which the company believes can be an effective treatment against some forms of cancer. Repair Biotechnologies’ second major project relates to atherosclerosis, which is caused by the accumulation of intracellular waste in arteries. While present therapies focus on reducing cholesterol, Repair Biotechnologies has licensed a technology to make the macrophage cells responsible for repairing arteries resilient to excess cholesterol, and thus able to repair atherosclerotic damage.

“SENS Research Foundation was founded to push forward proof-of-concept work demonstrating the validity of the SENS paradigm to the point at which people can actually do something with it. Now we’re seeing some of these technologies getting the recognition from investors that they deserve, which in turn is driving critical growth in the private-sector side of the field,” said Aubrey de Grey, co-founder and Chief Science Officer of SENS Research Foundation. “I’m thrilled to see Repair Biotechnologies taking things in this area to the next level.”

Nothing in this post should be construed as an offer to sell, or a solicitation of an offer to buy, any security or investment product. Certain information contained herein may contains statements, estimates and projections that are “forward-looking statements.” All statements other than statements of historical fact in this post are forward-looking statements and include statements and assumptions relating to: plans and objectives of Repair Biotechnologies’ management for future operations or economic performance; conclusions and projections about current and future economic and political trends and conditions; and projected financial results and results of operations. These statements can generally be identified by the use of forward-looking terminology including “may,” “believe,” “will,” “expect,” “anticipate,” “estimate,” “continue”, “rankings” or other similar words. Repair Biotechnologies does not make any representations or warranties (express or implied) about the accuracy of such forward-looking statements. Accordingly, you should not place reliance on any forward-looking statements.

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Why Children Are Getting Fatty Liver Disease

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Fatty liver disease is caused by excess fat in your liver. The medical term is hepatic steatosis. Your liver normally contains some fat, but when greater than 10% of the weight of the liver is fat, it’s called fatty liver. There are two main types: nonalcoholic fatty liver disease (NAFLD) and alcoholic fatty liver disease, also called alcoholic steatohepatitis.1

NAFLD may be suspected if a blood test shows higher levels of liver enzymes than expected. While the disease is found more frequently in adults, researchers are finding NAFLD is a growing concern in the pediatric community, which triggered at least one intervention study weaning participants off sugar to reduce obesity and Type 2 diabetes.2

Chief of gastroenterology, hepatology and nutrition at University of Southern California and Children’s Hospital of Los Angeles (CHLA), Dr. Rohit Kohli, commented,3 “Fatty liver disease is ripping through the Latino community like a silent tsunami and especially affecting children.”

While research demonstrates 25% in the U.S. have fatty liver disease,4 in the Latino community the rate is much higher. One study in Dallas, Texas5 examined 2,287 subjects from a multi-ethnic population and found 45% of Hispanics suffered from fatty liver disease. The ethnic differences in the frequency of disease in this study mirrors those in past studies for NAFLD-related cirrhosis.

Key Facts About Fatty Liver Disease

NAFLD is the type not related to heavy alcohol use and in this category there are two types: simple fatty liver, in which your liver has additional fat but little to no inflammation or damage, and nonalcoholic steatohepatitis (NASH), in which you suffer from inflammation and damage in the liver cells, as well as excess fat in your liver.

NASH may cause fibrosis or scarring of the liver and lead to cirrhosis or liver cancer. Researchers have not been able to point to a single cause of NAFLD, but they do know it occurs more commonly in those who have specific risk factors, including:6,7

Type 2 diabetes or prediabetes

Metabolic disorders, including metabolic syndrome

High levels of fats in the blood

Obesity

Middle-aged or older

High blood pressure

Rapid weight loss

Infections, such as hepatitis C

Exposure to some toxins

Gallbladder removal

Hispanic

NAFLD affects nearly 25% globally.8 However, as the rates of obesity and Type 2 diabetes rise, so do the rates of NAFLD. NAFLD is usually a silent disease, meaning most are unaware of the condition and have few or no symptoms. When symptoms are present, individuals may feel greater fatigue or have discomfort in the upper right-hand side of the abdomen.

It is important to distinguish between simple fatty liver disease and NASH since those with NASH experience damage to their liver cells, which increases the risk of progression to fibrosis, cirrhosis and liver cancer. According to Harvard Health Publishing,9 NASH cirrhosis is expected to top the reasons for liver transplants.

Sugar Passed in Breast Milk Predisposes Infants to Obesity

A new study10 is being led by Michael Goran, Ph.D., director of the diabetes and obesity program at Children’s Hospital Los Angeles. Last year, he discovered high fructose corn syrup (HFCS) sweetened beverages were passed through breast milk, potentially predisposing infants to fatty liver and obesity.11

Six weeks after giving birth, 41 participating women were randomized into two groups. One group consumed a readily available HFCS sweetened beverage and the other group consumed an artificially-sweetened control beverage. At each testing session, the mothers expressed milk every hour for six consecutive hours.

The researchers then measured the concentration of fructose, glucose and lactose in the breast milk. Changes were significant only for measurements of fructose, with comparisons showing HFCS beverages increased breast milk fructose at hour two, three, four and five hours after consumption. It is important to note breast milk normally does not contain fructose.12 Goran commented:13 

“Lactose is the main source of carbohydrate energy and breast milk is very beneficial, but it’s possible that you can lose some of that beneficial effect depending on maternal diet and how that may affect the composition of breast milk.

Other studies have shown that fructose and artificial sweeteners are particularly damaging during critical periods of growth and development in children. We are beginning to see that any amount of fructose in breast milk is risky.”

Dr. Robert Lustig, professor in the division of endocrinology at the University of California, is a pioneer in decoding sugar metabolism. He was among the first to bring attention to the fact that processed fructose is far worse for your metabolic system than other sugars. Fructose is broken down like alcohol in your body,14 triggering liver damage and causing mitochondrial and metabolic dysfunction.

This damage is very similar to that caused by ethanol and other toxins. Fructose also triggers severe metabolic dysfunction as it is readily metabolized into fat, far more so than other sugars. Researchers are finding exposure before birth may increase an infant’s risk of obesity leading to a higher risk of Type 2 diabetes and NAFLD.15

Gene Variant Increases Risk of Fatty Liver Disease

Before 2006, few knew children could develop NAFLD. Dr. Jeffrey Schwimmer, professor of pediatrics at the University of California San Diego, reviewed 742 autopsies of children and teenagers who had died from traumatic injury. He found an incidence of 13% with fatty liver disease, and 38% in those who were obese.16

The researchers concluded NAFLD was the most common liver abnormality in children aged 2 to 19. They suggested the identified risk factors should be considered in the development of protocols to screen children and adolescents who are at risk.

A study released in 200817 by a group of researchers from the University of Texas demonstrated a gene variant called PNPLA3 could increase the risk of fatty liver disease. Nearly 50% of Latinos have at least one copy of this high-risk gene, and 25% have two copies according to Goran.18

Goran then undertook another study, eventually demonstrating children as young as 8 who had two copies of PNPLA3 and who consumed high amounts of sugar had 2.36 times as much fat in their livers as children without the gene.19 In the clinical trial20 currently underway, his team first tests participating children for the gene and then uses an MRI to measure liver fat percentage.

The sugar consumption of the child is measured and cataloged and then a dietitian educates the family on the impact of sugar. The team does another MRI four months later to measure liver fat and assess the impact of the intervention.

Goran’s research and past studies21 have demonstrated early exposure to sugar and fructose likely contribute to obesity, diabetes and fatty liver disease as fructose enhances the body’s capacity to store fat.

Excess Fructose Triggers Obesity and Fatty Liver Disease

Results of a meta-review in Mayo Clinic Proceedings22 confirmed that not all calories are equal. The dogmatic belief that a calorie is a calorie has driven the weight loss industry and contributed to an ever-worsening history of health in the Western world.

Unfortunately, it continues to be a concept taught in schools, even though we now know it’s false. The source of the calories does indeed have a significant impact on your health and weight. In the review, the researchers evaluated how different calories affected health. As reported by Time Magazine:23

“What they found was that the added sugars were significantly more harmful. Fructose was linked to worsening insulin levels and worsening glucose tolerance, which is a driver for prediabetes. It caused harmful fat storage — visceral fat on the abdomen — and promoted several markers for poor health like inflammation and high blood pressure.

‘We clearly showed that sugar is the principal driver of diabetes,’ says lead study author James J. DiNicolantonio, a cardiovascular research scientist at Saint Luke’s Mid America Heart Institute. ‘A sugar calorie is much more harmful.'”

Another more recent study published in 201724 found fructose promotes complications in glucose metabolism and alters lipid profiles associated with an inflammatory response. The researchers found this implied a systemic picture of insulin resistance.

Choline Deficiency Also Plays a Key Role in Fatty Liver Disease

Choline is a compound in living tissue and is important in the synthesis and transportation of lipids (fats). It was discovered in 186225 and officially recognized as an essential nutrient in 1998.26

Several studies27,28 have linked higher intake of choline to a range of benefits and, in fact, it appears to be a key factor in preventing the development of fatty liver disease. By enhancing secretion of very low density lipoproteins (VLDL)29 in your liver, required to safely transport fat out, choline may protect your liver health.

Epigenetic mechanisms30 of choline also explain how it helps maintain healthy liver function. Dietary choline is an important modifier of DNA and modulates expression of many of the pathways involved in liver function.

Chris Masterjohn, who has a Ph.D. in nutritional sciences,31 proposes choline deficiency is a significant trigger of NAFLD and believes the rise in NAFLD is largely the result of rejecting liver and egg yolks in the diet:

“More specifically, I currently believe that dietary fat, whether saturated or unsaturated, and anything that the liver likes to turn into fat, like fructose and ethanol, will promote the accumulation of fat as long as we don’t get enough choline.”

In a 2010 article,32 Masterjohn reviews the medical literature supporting this view. The link between choline and fatty liver initially emerged from research into Type 1 diabetes. Studies in the 1930s demonstrated lecithin found egg yolk (containing high amounts of choline) could cure fatty liver disease in Type 1 diabetic dogs. They later found choline alone provided the same benefit.

More Ways to Support Your Liver Health

Hints to additional ways of supporting your liver health may be found in the commonly identified risk factors for NAFLD. In addition to reducing or eliminating processed fructose from your diet and including foods with choline, other modifiable factors that can have a significant impact on the development of NAFLD include:33,34

  • Maintaining a healthy weight — Managing a healthy weight requires more than monitoring your calorie intake and energy expenditure. For a full explanation of one of the master keys to healthy eating, see “My Updated Nutrition Plan — Your Guide to Optimal Health.”
  • Exercising regularly — Regular movement and exercise benefits your body by improving insulin sensitivity, supporting your metabolism and mitochondrial health, helping to manage weight and blood pressure, toning muscle and improving your balance. Exercise also improves your sleep quality, mood and mental health. There is a long list of benefits — including reducing your risk of NAFLD.
  • Limiting medications — Limit any medications to those necessary and follow dosing recommendations. Some medications increase your risk of NAFLD and other health conditions. Reduce those risks by making lifestyle changes to minimize your dependence on medications.
  • Managing high blood pressure — High blood pressure increases your risk of cardiovascular disease, dementia and NAFLD. There are several natural methods of reducing high blood pressure while working with your physician to wean off medication.
  • Reducing insulin resistance — Insulin resistance may lead to metabolic syndrome, prediabetes and Type 2 diabetes, all precursors to NAFLD. For an overview of insulin resistance and how to reduce your risk of metabolic disease, see my previous article, “Research Proves Causation — Sugar Consumption Increases Risk for Chronic Disease.”

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Why Splenda Is Not So Splendid, and Safety Has Been Questioned

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Are artificial sweeteners such as Splenda still part of your daily diet? If so, I would strongly recommend reconsidering. It’s important to realize that while artificial sweeteners have no (or very few) calories, they are still metabolically active,1 and not in a beneficial way.

For example, research2,3 published in the online version of the Journal of Toxicology and Environmental Health August 21, 2018, shows sucralose — sold under brand names such as Splenda, Splenda Zero, Zero-Cal, Sukrana, Apriva, SucraPlus, Candys, Cukren and Nevella — is metabolized and accumulates in fat cells.

Remarkably, artificial sweeteners have become so ubiquitous, research4 published in the April 2019 issue of Ecotoxicology and Environmental Safety refers to them as an “emerging” environmental contaminant, noting they have “high water persistence.”

According to this paper, artificial sweeteners are chemically stable in the environment and water supplies appear to be at greatest risk for contamination. The researchers looked at 24 environmental studies assessing the presence of artificial sweeteners in the environment from 38 locations around the world, including Europe, Canada, the U.S. and Asia.

“Overall, the quantitative findings suggested that the occurrence of non-nutritive artificial sweeteners is present in surface water, tap water, groundwater, seawater, lakes and atmosphere,” the paper states. What the ultimate ramifications for wildlife, especially marine life, and human health might be are still anyone’s guess.

Artificial Sweeteners Promote Obesity, Diabetes and Metabolic Syndrome

As explained in the 2016 paper,5 “Metabolic Effects of Non-Nutritive Sweeteners,” many studies have linked artificial sweeteners to an increased risk for obesity, insulin resistance, Type 2 diabetes and metabolic syndrome. This is in stark contrast to what you’re told by industry, which continues to promote artificial sweeteners as a way to lower your risk of those conditions.

The paper presents several mechanisms by which artificial sweeteners promote metabolic dysfunction:

1. They interfere with learned responses that contribute to glucose control and energy homeostasis — Studies have demonstrated that when sweet taste and caloric intake are mismatched, your body loses its ability to properly regulate your blood sugar.

2. They interact with sweet-taste receptors expressed in digestive system that play a role in glucose absorption and trigger insulin secretion, thereby inducing both glucose intolerance and insulin resistance, which raises your risk of obesity. Sweet taste without calories also increases appetite6 and subjective hunger ratings.7

3. They destroy your gut microbiota — A 2008 study8 revealed sucralose (Splenda) reduced gut bacteria by as much as 49.8%, preferentially targeting bacteria known to have important human health benefits. Consuming as few as seven little Splenda packets may be enough to have a detrimental effect on your gut microbiome.

More recent research,9 published in the journal Molecules in October 2018, confirmed and expanded these findings, showing that all currently approved artificial sweeteners (aspartame, sucralose, saccharin, neotame, advantame and acesulfame potassium-k) disrupt the gut microbiome — in part by damaging the bacteria’s DNA, and in part by interfering with their normal activities.

Another 201810 found Splenda consumption may exacerbate gut inflammation and intensify symptoms in people with Crohn’s disease by promoting harmful gut bacteria. These results echoed those published in 2014,11 where they found Splenda may exacerbate symptoms of Crohn’s disease by augmenting “inflammatory activity at the biochemical level” and altering microbial-host interactions within the intestinal mucosa.

Similarly, research12 published in 2017 implicated sucralose in chronic liver inflammation by altering “the developmental dynamics of the gut microbiome.”

Why You Should Never Cook With Splenda

Splenda (sucralose) is frequently recommended for cooking and baking,13 and is often used in processed foods in which high heat was involved. This, despite the fact that scientists have warned about the dangers of heating sucralose for years.

In the 2013 paper,14 “Sucralose, a Synthetic Organochloride Sweetener: Overview of Biological Issues,” the authors state that “Cooking with sucralose at high temperatures … generates chloropropanols, a potentially toxic class of compounds.” This paper also warns the acceptable daily intake set for sucralose may in fact be hundreds of times too high to ensure safety.

The German Federal Institute for Risk Assessment (BfR) recently issued a report15 on the available data on sucralose, confirming that cooking with sucralose is likely a terrible idea, as chlorinated compounds are formed at high temperatures. As reported by MedicalXpress:16

“When sucralose (E 955) is heated to temperatures higher than 120 degrees C a gradual — and with further continuously increasing temperature — decomposition and dechlorination of the sweetener occurs.

Temperatures of between 120 degrees C [248 degrees Fahrenheit] and 150 degrees C [302 degrees F] are possible during industrial manufacturing and processing of foods, and are also reached in private households during cooking and baking of foods containing sucralose.

This may lead to the formation of chlorinated organic compounds with a health-damaging potential, such as polychlorinated dibenzo-p-dioxins (PCDD), dibenzofurans (PCDF) and chloropropanols.”

Chloropropanols, while still poorly understood, are believed to have adverse effects on your kidneys and may have carcinogenic effects.17 One good reason to be suspicious of chloropropanols is because they’re part of a class of toxins known as dioxins, and dioxins are known to cause cancer and endocrine disruption.

The fact that sucralose creates toxic dioxins when heated is also a concern for those who use vaping liquid containing this artificial sweetener. A 2017 study18 found sucralose contributes sweet taste only when used in a cartridge system, and chemical analysis showed the use of a cartridge system also raised the concentration of sucralose in the aerosol.

I find it interesting that these studies are now confirming what I suspected and published in my book, published over 10 years ago — “Sweet Deception” — which was an expose on Splenda.

Sucralose Shown to Have Carcinogenic Potential

Research19 published in 2016 in the International Journal of Occupational and Environmental Health tested the carcinogenic potential of sucralose by adding it to mouse feed, at various concentrations, starting at 12 days of gestation and continuing throughout their natural life span.

Results showed male mice experienced a significant dose-related increase in malignant tumors and hematopoietic neoplasias (cancer of the blood, bone marrow and the lymphatic system). The dosages tested were 0, 500, 2,000, 8,000 and 16,000 parts per million (ppm). The worst results occurred in males given 2,000 ppm and 16,000 ppm. According to the authors:

“These findings do not support previous data that sucralose is biologically inert. More studies are necessary to show the safety of sucralose, including new and more adequate carcinogenic bioassay on rats. Considering that millions of people are likely exposed, follow-up studies are urgent.”

Pregnant Women Beware

More recent research,20 published in 2018, revealed the artificial sweeteners sucralose and acesulfame-potassium transfer into breast milk — a crucial fact that pregnant women need to be mindful of, considering the harmful effects of these compounds. To determine whether the sweeteners could transfer into breast milk, the researchers enrolled 34 women who were exclusively breastfeeding.

Each of the women drank 12 ounces of Diet Rite Cola, which contains 68 milligrams (mg) of sucralose and 41 mg of acesulfame-potassium, before breakfast. Habitual use of artificial sweeteners was also assessed via a diet questionnaire. Breast milk samples were collected before ingestion and every hour thereafter for six hours. As reported by the authors:

“Owing to one mother having extremely high concentrations, peak sucralose and acesulfame-potassium concentrations following ingestion of diet soda ranged from 4.0 to 7387.9 ng/mL and 299.0 to 4764.2 ng/mL, respectively.”

This is believed to be the first time researchers have demonstrated that infants are in fact exposed to artificial sweeteners even when exclusively breastfed (if the mother consumes them). An accompanying commentary21 by pediatric experts notes:

“NNS [non-nutritive sweeteners] were present in the breast milk of all subjects in physiologically significant amounts, and … at concentrations well above the taste thresholds. Why is this important?

NNS or non-caloric artificial sweeteners (NCAS) are ubiquitous in the modern diet … Despite the approval by the FDA and European Food Safety Authority, concerns, admittedly largely unproven, persist about their safety … The concerns about NNS are three-fold.

First, that they may adversely alter taste preferences. Second, that the ultimate effect may be contrary to what is intended and their ingestion may increase food consumption. Third, that they may adversely alter the gut bacterial microbiome and its metabolites.

All of these concerns are magnified with early exposure in life. The evidence to support these concerns is either inductive or based on experimental models and emerging human data.”

‘Diet’ Beverages Linked to Increased Risk of Stroke and Heart Attack

Another 2018 study22 by the American Heart Association (AHA) found that, compared to drinking none or just one “diet” drink per week, women over 50 who drank two or more artificially sweetened beverages per day had a:23

  • 31% increased risk for ischemic stroke
  • 29% increased risk of coronary heart disease
  • 23% increased risk of all types of stroke
  • 16% increased risk of early death

The risk is particularly high for women with no previous history of heart disease, those who are obese and/or African-American women. The study included more than 81,714 women from the Women’s Health Initiative Observational Study, a longitudinal study of the health of 93,676 postmenopausal women between the ages of 50 and 79. The mean follow-up time was close to 11.9 years. According to the authors:

“In women with no prior history of cardiovascular disease or diabetes mellitus, high consumption of ASB [artificially-sweetened beverages] was associated with more than a twofold increased risk of small artery occlusion ischemic stroke … High consumption of ASBs was associated with significantly increased risk of ischemic stroke in women with body mass index ≥30 …”

In an accompanying editorial,24 “Artificial Sweeteners, Real Risks,” Hannah Gardener, assistant scientist in the department of neurology at the University of Miami, and Dr. Michell Elkind at Columbia University, suggest drinking pure water instead of no-calories sweetened beverages, as it is by far the safest and healthiest low-calorie drink there is.

If you want some flavor, just squeeze a little bit of fresh lemon or lime into mineral water. In instances where your cooking, baking or beverage needs a little sweetener, be mindful of your choice.

Sucralose Linked to Liver, Kidney and Thymus Damage

Other recent research25 published in the journal Morphologie found sucralose caused “definite changes” in the liver of treated rats, “indicating toxic effects on regular ingestion.” The researchers warn these findings suggest sucralose should be “taken with caution to avoid hepatic damage.”

In other words, regularly using Splenda could damage your liver. Here, adult rats were given a much higher (yet nonlethal) oral dose of sucralose — 3 grams (3,000 mg) per kilo body mass per day for 30 days, after which the animals’ livers were dissected and compared to the livers of unexposed controls. According to the authors:

“Experimental rats showed features of patchy degeneration of hepatocytes along with Kupffer cells hyperplasia, lymphocytic infiltration, sinusoidal dilatation and fibrosis indicating a definite hepatic damage on regular ingestion of sucralose. Sinusoidal width was also found to be increased in experimental animals as compared to controls.”

Studies have also linked sucralose consumption to liver and kidney enlargement26,27 and kidney calcification.28,29 Another organ affected by sucralose is your thymus, with studies linking sucralose consumption to shrinkage of the thymus (up to 40%30,31) and an increase in leukocyte populations (immune system cells) in the thymus and lymph nodes.32

Sucralose Safety Has Been Repeatedly Questioned

At the time of this writing, there are 27,400 references to sucralose in the scientific search engine Google Scholar, so there’s no shortage of studies to review if you’re curious. Here’s a small sampling of papers raising questions about the safety of this artificial sweetener.

Artificial Sweetener Such as Sucralose May Promote Inflammation in Human Subcutaneous Fat-Derived Mesenchymal Stromal Cells, 2017 33 Research presented at GW Annual Research Days in 2017 shows sucralose consumption caused an increase in superoxide accumulation and cellular inflammation.

The sweetener also Increased expression of a specific sweet taste receptor. According to the researchers, “upregulation of adipogenic genes … cultured in near physiological concentrations of sucralose, indicate possible causality between increased fat deposition and sweetener use.”

The Non-Caloric Sweeteners Aspartame, Sucralose and Stevia sp. Induce Specific but Differential Responses to Compartmentalized Adipose Tissue Accumulation, 201734 In this study, consumption of sucralose resulted in weight gain, elevated blood glucose and body fat accumulation.

Sucralose Activates an ERK1/2–Ribosomal Protein S6 Signaling Axis, 201635 Sucralose was found to stimulate insulin secretion much like glucose, but through completely different and poorly understood pathways. According to the authors, these findings “will have implications for diabetes.”

Changes in the Expression of Cell Surface Markers in Spleen Leukocytes in a Murine Model of Frequent Sucralose Intake, 201636 This study found frequent sucralose intake may affect your immune function. According to the authors:

“Our results show a decrease in the frequency of B lymphocyte population and T lymphocytes in comparison to the control group. In B and T lymphocytes the analysis of co-stimulatory molecules show a lower frequency compared to the control group. The immune response depends on the differentiation and activation of cellular populations.

We hypothesized that chronic ingestion of commercial sucralose might be affecting the immune response by modifying the frequencies of cellular populations, as well as the expression of co-stimulatory and inhibitory molecules … by decreasing the ability of co-stimulation between B an T lymphocytes, with a probable effect on the immune response.

It is necessary to further determine if sucralose intake affects the efficiency of the immune response.”

Popular Sweetener Sucralose as a Migraine Trigger, 200637 As noted by the authors, “This observation of a potential causal relationship between sucralose and migraines may be important for physicians to remember this can be a possible trigger during dietary history taking.

Identifying further triggers for migraine headaches, in this case sucralose, may help alleviate some of the cost burden (through expensive medical therapy or missed work opportunity) as well as provide relief to migraineurs.”

Healthier Sugar Substitutes

Two of the best sugar substitutes are Stevia and Lo Han Kuo (also spelled Luo Han Guo). Stevia, a highly sweet herb derived from the leaf of the South American stevia plant, is sold as a supplement. It’s completely safe in its natural form and can be used to sweeten most dishes and drinks.

Lo Han Kuo is similar to Stevia, but is my personal favorite. I use the Lakanto brand vanilla flavor which is a real treat for me. The Lo Han fruit has been used as a sweetener for centuries, and is about 200 times sweeter than sugar.

A third alternative is to use pure glucose, also known as dextrose. Dextrose is only 70% as sweet as sucrose, so you’ll end up using a bit more of it for the same amount of sweetness, making it slightly more expensive than regular sugar. It is safer than regular sugar, which is 50% fructose.

Still, it’s well worth it for your health as it does not contain any fructose whatsoever. Contrary to fructose, glucose can be used directly by every cell in your body and as such is a far safer sugar alternative.

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Giving a Name to Age-Related TDP-43 Proteopathy

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Much of the spectrum of age-related neurodegenerative conditions is associated with, and at least partly caused by, the accumulation of abnormal proteins or protein aggregates in the brain. These include the α-synuclein associated with Parkinson’s disease, the amyloid-β and tau of Alzheimer’s disease, and so forth. This sort of condition, in which malformed proteins are a contributing cause, is termed a proteopathy. A more recently recognized neurodegenerative proteopathy involves the TDP-43 protein, and the evidence for its relevance to age-related dementia has reached the point at which researchers and administrators now feel that they can advocate for greater recognition and funding for research and development in this part of the field.


Alzheimer’s is the most common form of dementia, which is the loss of cognitive functions – thinking, remembering, and reasoning – and everyday behavioral abilities. In the past, Alzheimer’s and dementia were often considered to be the same. Now there is rising appreciation that a variety of diseases and disease processes contribute to dementia. Each of these diseases appear differently when a brain sample is examined at autopsy. However, it has been increasingly clear that in advanced age, a large number of people had symptoms of dementia without the telltale signs in their brain at autopsy. Emerging research seems to indicate that the protein TDP-43 – though not a stand-alone explanation – contributes to that phenomenon.

TDP-43 (transactive response DNA binding protein of 43 kDa) is a protein that normally helps to regulate gene expression in the brain and other tissues. Prior studies found that unusually misfolded TDP-43 has a causative role in most cases of amyotrophic lateral sclerosis and frontotemporal lobar degeneration. However, these are relatively uncommon diseases. A significant new development seen in recent research is that misfolded TDP-43 protein is very common in older adults. Roughly 25 percent of individuals over 85 years of age have enough misfolded TDP-43 protein to affect their memory and/or thinking abilities.

TDP-43 pathology is also commonly associated with hippocampal sclerosis, the severe shrinkage of the hippocampal region of the brain – the part of the brain that deals with learning and memory. Hippocampal sclerosis and its clinical symptoms of cognitive impairment can be very similar to the effects of Alzheimer’s. “Recent research and clinical trials in Alzheimer’s disease have taught us two things: First, not all of the people we thought had Alzheimer’s have it; second, it is very important to understand the other contributors to dementia.” Scientists have now described the newly-named pathway to dementia as Limbic-predominant Age-related TDP-43 Encephalopathy, or LATE.

LATE is an under-recognized condition with a very large impact on public health. Researchers emphasized that the “oldest-old” are at greatest risk and, importantly, they believe that the public health impact of LATE is at least as large as Alzheimer’s in this group. The clinical and neurocognitive features of LATE affect multiple areas of cognition, ultimately impairing activities of daily life. Additionally, based on existing research, the authors suggested that LATE progresses more gradually than Alzheimer’s. However, LATE combined with Alzheimer’s – which is common for these two highly prevalent brain diseases – appears to cause a more rapid decline than either would alone.

Link: https://www.nia.nih.gov/news/guidelines-proposed-newly-defined-alzheimers-brain-disorder

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Boosting Levels of NAD+ May Make Senescent Cells More Aggressively Inflammatory

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Enhancing levels of NAD+ in mitochondria via delivery of various precursor compounds as supplements is growing in popularity as an approach to boost faltering mitochondrial function and thus modestly slow the progression of aging. A human trial demonstrated improved vascular function as a result of nicotinamide riboside supplementation, for example. Researchers here show that increased NAD+ will likely make worse the inflammatory signaling of senescent cells, however. Senescent cells accumulate with age, and are an important cause of the chronic inflammation of aging that drives the progression of many age-related diseases.

The results here suggest that efficient senolytic treatments to selectively destroy senescent cells should proceed any of the current approaches to raising levels of NAD+ in older individuals – and it is an open question as to whether any of the existing available options are efficient enough to make NAD+ enhancement safe in the longer term. Those people self-experimenting with NAD+ precursor supplementation should consider keeping a close eye on markers of inflammation.


Cellular senescence is a stable growth arrest that is implicated in tissue ageing and cancer. Senescent cells are characterized by an upregulation of proinflammatory cytokines, which is termed the senescence-associated secretory phenotype (SASP). NAD+ metabolism influences both tissue ageing and cancer. However, the role of NAD+ metabolism in regulating the SASP is poorly understood. Here, we show that nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme of the NAD+ salvage pathway, governs the proinflammatory SASP independent of senescence-associated growth arrest.

NAMPT expression is regulated by high mobility group A (HMGA) proteins during senescence. The HMGA-NAMPT-NAD+ signalling axis promotes the proinflammatory SASP by enhancing glycolysis and mitochondrial respiration. HMGA proteins and NAMPT promote the proinflammatory SASP through NAD+-mediated suppression of AMPK kinase, which suppresses the p53-mediated inhibition of p38 MAPK to enhance NF-κB activity. We conclude that NAD+ metabolism governs the proinflammatory SASP. Given the tumour-promoting effects of the proinflammatory SASP, our results suggest that anti-ageing dietary NAD+ augmentation should be administered with precision.

Link: https://doi.org/10.1038/s41556-019-0287-4

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Weekly Health Quiz: Zinc, Stress and Back Pain

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1 The following nutrient has been shown to contribute to improved behavior in children with attention deficit-hyperactivity disorder (ADHD):

  • Zinc

    A number of studies have found children afflicted with attention deficit-hyperactivity disorder (ADHD) are more likely to be zinc-deficient than other children, and zinc supplementation has been shown to contribute to improved behavior in children with ADHD. Learn more.

  • Vitamin C
  • Carbohydrates
  • Lectins

2 Cellular repair and regeneration occurs during which of the following fasting phases?

  • Within first 12 hours of fasting
  • The initial refeeding

    Cellular repair and regeneration occur when you start eating again, which is why cycling in and out of fasting and feasting is so imperative. The breakdown process occurs in the absence of food, while rebuilding occurs when food is reintroduced. Learn more.

  • Within first 16 to 18 hours of fasting
  • Several days after refeeding

3 BPA, dioxin, atrazine, phthalates, fire retardants, lead, mercury, PFCs and organophosphate pesticides are all examples of:

  • Volatile organic compounds
  • Radioactive materials
  • Endocrine disrupting chemicals

    BPA, dioxin, atrazine, phthalates, perchlorate, fire retardants, lead, mercury, arsenic, PFCs, organophosphate pesticides and glycol ethers are 12 of the worst and most widely used endocrine disrupting chemicals. Learn more.

  • Warfare agents

4 The following condition has been scientifically linked to an increased risk of cardiovascular disease, heart attack and stroke:

  • Autism
  • Eating disorders such as anorexia and bulimia
  • Narcissistic personality disorder
  • Chronic stress and stress related disorders such as acute stress reaction, post-traumatic stress disorder and adjustment disorder

    Stress can raise your risk of heart disease, heart attack and stroke via several different mechanisms. Recent research shows people with stress related disorders are 37 percent more likely to develop cardiovascular disease compared to the general population. Learn more.

5 The following is an independent risk factor for ill health and premature death and a primary contributor to back pain:

  • Prolonged sitting

    Excessive sitting contributes to back pain and is an independent risk factor for ill health and premature death. Foundation Training exercises — simple yet powerful structural movements that help strengthen and realign your posture — can help compensate for long hours spent sitting and significantly reduce back pain. Learn more.

  • Prolonged standing
  • Daily running
  • Strength training at the exclusion of aerobic training

6 Recent research shows outbreaks of this disease is spreading into areas in the U.S. and other countries where it has not been prevalent before:

  • Measles
  • Lyme disease

    Since Lyme disease became a nationally notifiable condition in 1991, the number of U.S. counties considered at high risk for Lyme disease has increased by more than 300 percent. The disease is also expanding rapidly all over the world, as new research presented in April 2019 shows that the outbreaks are creeping steadily into northern countries with less temperate climates. Learn more.

  • Ebola
  • West Nile virus

7 The following is a major reason why sun exposure lowers your risk of heart disease:

  • Sun exposure triggers release of serotonin.
  • Sun exposure raises your blood pressure.
  • Sun exposure triggers your body’s production of nitric oxide.

    Many of the benefits of sunlight, such as a decreased risk of heart disease, have to do with its ability to increase nitric oxide production in your body. Learn more.

  • Sunlight decreases your body’s production of nitric oxide.

 

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Rejuvenation Therapies Will Also Have Cycles of Hope and Disillusionment

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Every new class of rejuvenation therapy, and there will be many of them in the decades ahead, will follow a cycle consisting of a few years of rapidly growing hype, followed by a sharp crash of disappointment, and then, ultimately, long years of slow and steady success. People attach great hopes to the early stages of every new technology, unrealistic expectations for sweeping, immediate change and benefit. Those expectations are usually possible to realize in the long term, but they can only be met in the later stages of development, perhaps several decades after the advent of the new approach to rejuvenation. Producing a mature product that meets the early visions needs the participation of an entire industry, much of which typically does not exist at the start of the process.

Every new technology goes through this cycle, lasting decades from start to finish. The life span of a technology is perhaps fifty years, depending on where one wants to draw the line between a given technology and its next generation, and the first decade can be quite the wild ride when it comes to raised expectations and sudden disillusionment. Human beings are just built this way, the incentives operating at every step of the development process produce this outcome regardless of the fact that we’ve all seen it before.

Nothing happens quickly, even when the course of action is obvious, even when proof of principle exists for a new medical technology. This is the result of the way in which investment and commercial development works in practice, as it is based on a great deal of happenstance in the percolation of new information through communities, as well as the process of finding, organizing, and persuading groups of people. It takes a few years for a potential entrepreneur to move from exposure to concept to launching a startup company. It takes a few years for a company to succeed or fail. It takes a few years for those lessons to percolate through the research and development communities. Similar cycles play out in the grant writing and publish or perish world of research. Several of these cycles may be needed for any new technology to launch in a useful form. This is why even comparatively straightforward advances can take a decade to make their way out of the labs. Nothing is really all that simple in practice, and regulation slows down these cycles of progress in medicine in comparison to other industries.

Why do the early years of development, those leading in to the first clinical therapies for a new medical technology, inevitably involve an excess of hype? Well, firstly it is sufficiently challenging to raise funds for research in the early stages that advocates tend to sell the vision of the complete industry, the end product rather than the first versions. Further, in the world of biotech startups and venture capital, near all investors are looking for the seeds of enormous, industry-changing companies, the big wins that will provide enormous returns on investment. All venture funds provide their investors with returns that are largely derived a couple of big wins amidst the failures and the mere successes, and the financial model for such funds is predicated on finding those few big wins. This cultivates, directly and indirectly, a culture of public relations and industry commentary that is prone to hype, to emphasizing the facts in ways that are attractive to investors. Lastly, the people who would benefit from rejuvenation therapies, or indeed any radical new advance the capabilities of medical science, rarely have a good understanding of the realities of and the underlying science, and can muster an enormous degree of hope on that basis.

It is worth considering that the development of therapies is in fact a difficult and challenging process in its details. It involves a great deal of discovery as matters move from cells to mice to human trials. The early stem cell therapies of fifteen to twenty years ago were an example of the type, in that the simple transplantation of stem cells did not led to the reliable regenerative therapies that were hoped for at the outset, cures that would reverse heart disease and numerous other age-related conditions. These hope led to the establishment of countless clinics and a sizable medical tourism industry. Obstacles were discovered, in the form of the sizable logistical costs, the difficulties in standardizing cells for therapy, the unreliably benefits when it comes to regeneration. Transplanted stem cells do not survive for long, and it is their temporary signaling that produces benefits, changing for a time the behavior of native cells and tissues. After the initial years of work, the results consist of a few standardized approaches that fairly reliably reduce chronic inflammation for a time, a considerably benefit, but that fail to reliably improve tissue function and structure. This is a lesser outcome by far than the goals aimed at by the early advocates and developers.

The development catches up to the early hype, however. It just takes time. Presently the field of stem cell research and development is well on the way towards approaches that are in principle capable of reliably producing regeneration. Some of those are quite similar to the early visions, the transplantation of cells that survive in large numbers to integrate with tissues and improve their function. They result from incremental, steady advances in capabilities, rather than any profound new approach to the problem. Others are indeed entirely novel lines of work that didn’t exist, even in concept, at the turn of the century, such as the use of full or partial reprogramming to produce patient-specific or universal cell lines, or even to alter cells in vivo.

The world turns, and we live in an age of change, a revolution in progress in the capabilities of biotechnology and its application to medicine. It just doesn’t happen quite as rapidly as everyone would like it to.

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Are Standard Lipid Profile Tests Enough? Advanced Cholesterol Testing

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Are Standard Lipid Profile Tests Enough? Advanced Cholesterol Testing
With heart disease being a leading cause of death among Americans, you may be wondering: How healthy is my heart?

You eat right, exercise and know how to manage stress. Your annual physical includes the standard blood tests, including a lipid (cholesterol) profile to evaluate heart disease risk, cholesterol (HDL and LDL) and triglycerides. Your blood pressure and electrocardiogram (ECG) results may be normal. Everything looks OK, so there’s nothing to worry about . . . right?

A standard lipid panel that tests for serum total cholesterol, high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL) and triglycerides is a necessary part of regular blood work and a way to screen for factors that contribute to heart disease. But there are other blood tests available that provide a much clearer picture of where you stand heart-health-wise.

Listen to Life Extension’s Michael A. Smith, MD, and Crystal Gossard, DCN, CNS®, LDN, as they bring their audience up-to-date on the latest tests for cholesterol and more on the Live Foreverish Podcast.

Advanced heart tests

There’s more to cholesterol than HDL and LDL.

Cholesterol, an important fat-like substance found in all cells, is needed to produce steroid hormones and forms a part of cell membranes, among other functions. Although some cholesterol is provided by the diet, most is made by the liver. Cholesterol is transported by low-density lipoprotein to tissues, while high-density lipoprotein delivers excess cholesterol back to the liver, where it is broken down and eventually excreted. Having an HDL level of 50 mg/dL or higher, an LDL level of less than 80 mg/dL and fasting triglycerides that are lower than 100 mg/dL is optimal for most individuals without other risk factors.

What are the best blood tests for predicting heart problems?

One of the best tests you can take is the NMR Lipoprofile® test, which measures the standard lipid levels in addition to LDL particle size and number. Low-density lipoprotein should be large, fluffy and buoyant (described as pattern A) as opposed to small and dense (described as pattern B). Small, dense LDL particles are likelier to infiltrate the arterial wall, leading to plaque formation. They are therefore a good marker for predicting cardiovascular disease.1 The NMR Lipoprofile® test also provides an assessment of insulin resistance that can help detect the risk of type 2 diabetes, a disease that increases the risk of cardiovascular disease.2

Apolipoproteins bind fat and cholesterol to form lipoproteins. While there are a number of apolipoprotein classes, the ones we’re going to look at are apolipoprotein A and apolipoprotein B. Apolipoprotein B (ApoB) is a component of some of the “unhealthier” lipoproteins, including low-density lipoprotein (LDL), very low-density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL) particles. Apolipoprotein A1 (ApoA1) is a component of high-density lipoprotein (HDL) particles and is potentially helpful in reducing build-up of arterial plaque. The Apolipoprotein Assessment, which measures apolipoprotein B and apolipoprotein A1, is important because the ApoB-to-ApoA1 ratio has a stronger association with cardiovascular disease risk than better-known lipoprotein cholesterol fractions.3

Best Blood Tests for Heart Disease Detection: Does LDL Matter?

Yes, knowing one’s LDL level is of vital importance in assessing one’s risk of cardiovascular disease. Testing for oxidized lipoproteins is also important. Oxidized LDL can be compared to rancid fat that is likelier to trigger inflammation and plaque formation than LDL that is not oxidized. Increased serum or plasma oxidized LDL is a marker for coronary artery disease.4

Tests for inflammation are valuable in the assessment of cardiovascular disease risk. While C-reactive protein (CRP) is a better-known test for systemic inflammation, myeloperoxidase (an immune system enzyme that is a biomarker of oxidative stress) testing can assess inflammation specific to the arterial wall. Testing for CRP and myeloperoxidase may be as important as cholesterol levels to evaluate the risk of cardiovascular disease.5

Another advanced heart test is the PLAC® test for lipoprotein-associated phospholipase A2 protein (Lp-PLA2) activity. Lp-PLA2 is a vascular inflammatory marker that plays an important role in the formation of arterial plaque that is vulnerable to rupture.6 This test measures the function of Lp-PLA2 in the walls of the arteries to help predict the risk of coronary heart disease events.

Heart tests for chest pain

Chest pain should be immediately evaluated. Although it may not always be caused by a heart attack, it’s better not to take chances. An ECG is usually the first test that is administered to people complaining of chest pain. This test measures the heart’s electrical activity and can reveal damage that has occurred.

Troponin is a protein that increases in the blood in response to damage to the heart muscle. This is measured in the emergency department following an ECG assessment of suspected heart attack. Troponin testing confirms acute heart attack diagnosis but does not indicate the mechanism of damage inflicted upon the heart.7

Chest x-rays and CT scans are other tests that may be employed to evaluate individuals who report chest pain. They may be repeated at follow-up, along with ECG stress tests and/or an angiogram, which enables visualization of the heart’s arteries.

Chest pain that comes and goes

Chest pain that comes and goes over an extended period of time may not be due to a heart attack but should still be evaluated by a physician. There are a number of tests and procedures that can help identify the cause of chest pain.

Availing yourself of some of these advanced tests can provide a more complete picture of heart health than standard blood tests. If an increased risk of cardiovascular disease is identified, preventive measures can be taken. By proactively assessing your risk factors, you can act immediately to reduce the risk of becoming one of the casualties of the world’s leading cause of death.

About Live Foreverish: Join Dr. Mike as he sits down with some of today’s leading medical, health and wellness experts to discuss a variety of health-related topics. From whole-body health to anti-aging and disease prevention, you’ll get the latest information and advice to help you live your life to the fullest. If you like what you hear, please take a moment to give Live Foreverish a 5-star rating on iTunes!

References

  1. Ivanova EA et al. Oxid Med Cell Longev. 2017;2017:1273042.
  2. Balakumar P et al. Pharmacol Res. 2016 Nov;113(Pt A):600-609.
  3. Walldius G et al. J Intern Med. 2006 May;259(5):493-519.
  4. Holvoet P et al. Arterioscler Thromb Vasc Biol. 2001 May;21(5):844-8.
  5. Heslop CL et al. J Am Coli Cardiol. 2010; 55: 1102-1109.
  6. Kolodgie FD et al. Arterioscler Thromb Vasc Biol. 2006 Nov;26(11):2523-9.
  7. Foy AJ et al. Med Clin North Am. 2015 Jul;99(4):835-47.

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Why You Should Embrace Healthful Sun Exposure

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Marc Sorenson, who has a doctorate in education, and who is the founder of the Sunlight Institute,1 has written an excellent book, “Embrace the Sun,” in which he reveals why sunlight is foundational for optimal health and longevity.2 While vitamin D supplements clearly have their place, you cannot obtain all the benefits you get from the sun when you swallow it.

For example, many of the benefits of sunlight, such as a decreased risk of heart disease, have to do with its ability to increase nitric oxide (NO) production in your body.3 Ultraviolet A (UVA) and the near-infrared light spectrum both increase NO, so you’re getting that benefit from both ends of the light spectrum. Fifty percent of sunlight is near-infrared.4

Near-infrared also increases cytochrome c oxidase (COO),5 the fourth cytochrome in the mitochondria, and neither of these benefits can be had from swallowing a pill. It’s really important to realize that your body is designed to benefit from sun exposure, and if you’re diabetic or have heart disease, it may well be one of the missing factors. As noted by Sorenson:

“When we get out in the sun, the research is incredible. The risk of heart disease and the risk of myocardial infarction drop dramatically in the summertime, and go up dramatically in the wintertime.

Meaning, there’s something there that has to be beyond vitamin D, because the vitamin D supplement studies with heart disease haven’t worked out well. What we know now is the main mover to prevent heart disease is probably NO, which is a potent vasodilator. It opens them up.

Blood pressure can go down dramatically with regular sun exposure, which it does. Among people who are getting sunlight on a regular basis, the risk of dropping dead of a heart attack goes down rather dramatically …

You can produce 20,000 international units (IU) in 20 minutes of ideal unobstructed sun exposure on both sides of the body …  

How the Sun Avoidance Conspiracy Was Born

Importantly, for every death caused by diseases related to excessive sun exposure — such as common skin cancers (basal cell and squamous cell carcinomas) as well as some other uncommon diseases — there are 328 deaths caused by diseases related to sunlight deprivation,6 according to Sorenson’s data.

According to a 2013 study,7 for every skin cancer death in northern Europe, between 60 and 100 people die from stroke or heart disease related to hypertension alone. Knowing your risk of dying from heart disease or stroke is 80 times greater on average than from skin cancer should really put things into perspective.8 Clearly, sun avoidance is hardly the lifesaving strategy dermatologists make it out to be.

I’d always wondered why there was such an avid aversion of sun exposure within the dermatology community. It just doesn’t make any sense — until I read Sorensen’s book, in which he dissects the motivation behind this illogical stance. He explains:

“The powers of darkness, as I call them, are very highly invested in the sunscreen industry. About 70 percent of the funding comes from the sunscreen industry. Of course, with a dermatological society, they back those who produce sunscreens.

We’ve got a vast conspiracy with the sunscreen industry. That’s one of the main things. Besides … medicine in general is not that interested in keeping people well, because if they do get people well — and sunlight will do that to a great extent — they’re out of business. There is a conspiracy out there. I’ve written a very large chapter about that and how they used their anti-sun [propaganda] to keep people sick.”

On Skin Cancer

There are two basic types of skin cancer: melanoma and nonmelanoma. Importantly, 75 percent of all melanoma occurs on areas of the body that never see the sun, Sorenson notes, and indoor workers have double the rate of lethal melanoma skin cancer than outdoor workers.9 A primary risk factor for melanoma appears to be intermittent sun exposure and sunburn, especially when you’re young.

According to data presented in his book, in 1935 about 1 in 1,500 people contracted melanoma. As of 2002/2003, that rate was 1 in 50. Between 2006 and 2015, melanoma rates increased 3 percent per year,10 so rates just keep going up.

“The more we use sunscreen, the more melanoma we get. Australia’s proven that for many, many years,” Sorenson says. “They use more sunscreen than any people on Earth, yet they have the highest prevalence of melanoma …

Melanoma increased by 3,000 percent between 1935 and, let’s say, 2002 to 2003. That’s a tremendous increase. Sun exposure during that time, by my government figures, has gone down by over 90 percent. We have a 90-percent decrease in sun exposure and a 3,000-percent increase in melanoma.

How does that add up for their theory? It doesn’t add up at all. They’re now beginning to realize that, I think, little by little. But still, they’re in that hip pocket of the medical schools that promote sunscreens and such.”

As noted by Sorenson, the sun actually protects you from melanoma. It does not protect again the more common skin cancers, though. However, protection from those can be had from a diet high in antioxidants.

Sun Avoidance Kills Far More People Than Sun-Related Diseases

Nonmelanoma skin cancers are primarily divided into basal cell and squamous cell cancer, and sun exposure does increase your risk of those cancers. The thing to remember is that these are typically nonlethal. The relative safety of skin cancer is craftily hidden, however, by combining statistics for nonfatal and fatal skin cancers.

Most of the deaths attributed to nonmelanoma skin cancers (basal and squamous cell), which number around 4,420 per year, according to cancer.net,11 are in those who have severely compromised immune systems. Melanoma, meanwhile, kills an estimated 7,230 people per year in the U.S.12,13 It’s also important to realize that common skin cancer does not turn into the deadlier melanoma.

When you consider the statistics, it seems clear that sun avoidance is actually increasing your risk of deadly skin cancer, and that by exposing your skin to the sun, you will decrease your risk of melanoma.

What’s more, sun avoidance will also raise your risk of internal cancers, along with a long list of chronic diseases, the mortality rates of which are far more alarming than melanoma. As mentioned earlier, for every sun-related death there are 328 deaths from sun-deficiency-related diseases.

Sorenson’s book also cites Iranian research showing women who cover themselves completely have a 10-times higher risk of breast cancer compared to women who don’t cover themselves completely. That’s a 1,000-percent greater risk of breast cancer. Yet women are being told to avoid sun exposure at all costs to protect their health.

You Can Benefit From Sun Exposure Year-Round

During wintertime at latitudes above 22 degrees you’re not going to be able to get enough ultraviolet B (UVB) exposure on your skin to significantly raise your vitamin D level, unless you are at high altitudes in the mountains.

However, you’re still getting other photoproducts such as brain-derived neurotrophic factor (BDNF), NO and others. They will be produced even in the winter when the sunlight is too weak to trigger vitamin D production.

“I tan every day in St. George, Utah,” Sorenson says. “It may be 40 degrees F. outside; I step into the garage, so I’m protected from the breezes. I get out in the sun every day. It’s not doing me a bit of good for vitamin D, but I do have my own tanning bed. I can go into that tanning bed and it produces a dramatic amount of vitamin D.

So will a good vitamin D sunlamp … Sometimes I fudge and take a vitamin D pill, but I would rather [use my tanning bed] because it’s a lot more natural than taking a vitamin D pill, in my opinion. That’s the way that I do it …

Of course, tanning beds have been much maligned, [yet it] dramatically increases bone strength. It dramatically increases vitamin D levels. It reduces the risk of psoriasis and eczema. It does many other things that they never give any credit for …

I was just thinking about the new study on Parkinson’s disease, [which] showed people who are out in the bright sun daily, regularly have 1/50th the risk of ever getting Parkinson’s. That’s fairly new research. I was stunned by that research.”

Avoid Sunburn at All Costs

Naturally, regardless of the season, you want to make sure you do not get sunburn. Once your skin turns the lightest shade of pink, move into the shade or put on clothing and a hat to cover up your skin. Beyond that point, there’s no benefit, only the risk of skin damage. As noted by Sorenson:

“Your body shuts it down at that point. In fact, your body will shut down your vitamin D production, along with anything else, that it doesn’t want. There is a very interesting piece of research … that shows people who use sunscreen have anywhere from three to six times the risk of sunburn.

Another one was a big meta-analysis, which showed there was no benefit whatsoever in using sunscreens. None at all. In fact, there was a slight increase in the risk of all skin cancers together.”

Sun Exposure Decreases Risk of Autoimmune Disease

Aside from lowering your risk for a variety of cancers, including melanoma, sun exposure also radically decreases your risk of autoimmune diseases. (Diseases in which your body identifies proteins and other structures made by the body as foreign and destroys them.) Two classic examples are multiple sclerosis (MS) and Type 1 diabetes.

Sorenson cites research from Finland showing vitamin D supplementation decreased the risk of Type 1 diabetes by five- to sixfold. When compared to Venezuelan children, who get ample sun exposure, Finnish children had 400 times the risk of Type 1 diabetes.

Researchers have also found an inverse risk between vitamin D status and MS risk,14 and studies have confirmed MS is far less prevalent in areas near the equator, such as Ecuador, where prevalence ranges from a low of 0.75 per 100,000 inhabitants in the South, to a high of 5.05 per 100,000 in the capital city of Quito.15

What’s a Healthy Vitamin D Level?

Science has shown 20 ng/mL (50 nmol/L), which is typically considered the cutoff for vitamin D sufficiency, is still grossly inadequate and dangerous to health. For optimal disease protection, you need a vitamin D blood level between 60 and 80 ng/mL16 (150 to 200 nmol/L).

Once you get above 60 ng/mL, the risk for cancer and other chronic illness declines dramatically — in the case of breast cancer by more than 80 percent.17

There appears to be variations in the ideal level, however, depending on the condition in question. Sorenson cites research showing that athletic performance, and the risk of injury due to falling among nonathletes, improved until they reached a level of about 63 ng/mL (158 nmol/L), at which point performance and risk of falling started to slightly decline again.

On the other hand, in the case of breast cancer, which is a major concern for women, levels upward of 80 ng/mL (200 nmol/L) appear to be the most protective. When aiming for those higher levels, though, I believe getting your vitamin D from sunlight becomes all the more important, especially if you’re seeking protection from diseases such as heart disease.

Because, remember, swallowing a vitamin D pill will not trigger NO production like sun exposure does, and increasing NO appears to be a significant way by which sun exposure lowers your heart disease risk. Sunlight also boosts your serotonin level, a neurotransmitter thought to play an important role in depression.

In his book, Sorenson cites research showing that spending the entire day in bright sunlight increases your serotonin level by 800 percent. A precursor to serotonin — melatonin — is also crucial for sleep and cancer prevention.

Sunlight and Visual Acuity

Myopia, with people needing glasses at an early age, and presbyopia, which is when you need reading glasses, are also on the rise, and this too may be a side effect of insufficient sun exposure. Sorenson explains:

“One of the studies was done comparing people in Singapore to people who grew up in Australia. They had the same ethnic background, basically Oriental-Asian background. Those who were playing in the sun in Australia had about one-sixth the risk of getting myopia.

It is so important. If we don’t get out and we don’t focus [our eyes] in the sun, [if] we don’t look into the distance — that may be one of the reasons we don’t get enough vitamin D, we don’t get enough serotonin, NO and any of the other photoproducts produced by the sun.

There is a pandemic of myopia. We’re seeing it here in the United States with the Asian kids. In many cases, as they get older, it will lead to blindness. Of course, they always talk about macular degeneration and so forth, but there’s a dichotomy here, because if you have macular degeneration, they tell you to totally stay out of the sun.

It does tend to relate to sun exposure. At the same time, vitamin D levels that are high tend to reduce the risk. So, what do you do? Stop getting your sun and take a vitamin D pill? I don’t think so. I think if we’re in the sun the way we ought to be and eat the polyphenols and so forth … that’s probably the way to prevent most of the older-age diseases.

Now, as far as presbyopia … I’ve had it since I was about 40. I just take some reading glasses and I can get along with reading my fine print. I wasn’t able to escape it. It runs in my family. I think there must be some genetic component there, because I was out in the sun and I never had any myopia.”

As for age-related macular degeneration (ARMD), which is the leading cause of blindness among the elderly, research by Dr. Chris Knobbe, an ophthalmologist who wrote a book on the risk factors of ARMD, whom I’ll be interviewing on this topic, has compiled massive amounts of data showing that ARMD did not exist before 1930 and this appears largely due to the consumption of processed foods, especially processed vegetable oils.

Sugar, of course, does not help either. That combination causes massive degeneration of your vision, which is very difficult to reverse in its advanced stages. But if you catch it at an early stage, you can reverse it using dietary changes.

For presbyopia, I recommend not wearing sunglasses and avoiding reading glasses. As you age, there’s a tendency to want to make that font bigger to see text better, but I recommend resisting that temptation, as it’s only going to make matters worse.

Also, avoid squinting and simply blink instead. Blink multiple times until the text becomes clear, then relax your eyes to refocus. Brighter light may also help you read without increasing the font size on your tablet or computer, or using reading glasses.

Sunlight for Bone Health

Sorenson also recounts some of the historical data supporting the idea that sun exposure benefits health in important ways and boosts athletic performance. Aside from breast health, research shows sun exposure also helps prevent osteoporosis, which is yet another significant concern for women in particular. Sorenson says:

“In Spain, women who were sun seekers, those who were always outside, trying to tan … as much as possible, those women had 1/11th the risk of ever having a hip fracture as women who were avoiding the sun. That one point alone should get every woman out in the sun, because all women are afraid not only of breast cancer but also of osteoporosis.

Women need sunlight to prevent it. Whether vitamin D pills will work, I am not convinced. They don’t give them enough vitamin D so they can’t really tell in the research. But we know that sunlight works to prevent hip fractures. Boy, that’s a big one to me …

[Higher] vitamin D levels also dramatically help your brain … People think better … You are 3.5 times more likely to end up in a rest home [assisted care facility] if you do not have a good vitamin D level … [If] you’ve got a mom, dad, uncle or whoever is in danger of going there, I think it can be prevented … They can stay at home, maybe with a son or daughter, and they wouldn’t need to worry about them injuring themselves every other second.”

More Information

To learn more, I strongly recommend picking up a copy of Sorenson’s book, “Embrace the Sun.” Strongly emphasized in the book is the importance of sunlight for the prevention of cardiovascular disease — again, by way of boosting NO, which lowers your blood pressure and increases blood flow, more so than raising your vitamin D.

Sorenson believes erectile dysfunction (ED), for men, may be a related problem that could be addressed through improved sun exposure, as one of the major reasons for ED is lack of NO. Cialis or Viagra is not the answer. Sunlight is.

“I think … we have to have holistic sun [exposure] again,” Sorenson says. “We need to have every single photoproduct produced. I have written down about five more photoproducts I haven’t even had the time to study. We don’t know what they do yet.

But why would you go for a vitamin D pill when you could get out in the sun and get all of the available [photoproducts] that we don’t even know [the benefits of] yet? For optimal human health, we need to be in the sunlight.”

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