The Question of a Limit to Human Life Span

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There has been much discussion in the aging research community these past few years on the topic of whether or not there is a limit to human life span, and how one might even go about defining such a thing. While life spans are in a slow upward trend due to general improvements in medical technology, can this trend continue without end, or will it run into a roadblock? In essence this is a debate over what can be extracted from poor data, and which data is in fact poor. Since there are few extremely old people, and since verifying age becomes ever harder the further back one has to go to search for records, the data for human mortality at advanced ages is very open to interpretation and reinterpretation, highly dependent on statistical methodologies used, and opinions on reliability of various sources of data.

In a more practical sense, this is all a storm in a teacup. Obviously there are mechanisms at work that ensure that even the statistical outliers don’t make it much past 120. Autopsies carried out on supercentenarians revealed transthyretin amyloidosis, and consequent heart failure, as the dominant cause of death. It is reasonable to hypothesize that this form of age-related damage ensures the effective upper limit on human life span – in the sense that there is no hard limit, but if critical organ dysfunction ensures that mortality rates are 50% yearly or higher, then the odds catch up pretty quickly.

Equally obviously, all of this is absolutely dependent on the present state of medical technology. If transthyretin amyloid can be broken down, such as via the theraputic approach developed by Covalent Bioscience, then the result will be that everyone who periodically undergoes the treatment will live longer. The same goes for clearance of senescent cells, and all the rest of the SENS program of ways to repair the causes of aging. If medical technology addresses the damage of aging, then the length of life changes.

A related topic is the question of whether or not mortality rates stop increasing in very late life. Studies show that extremely old flies stop aging, in the sense that aging is defined as an increase in mortality rate per unit time. The flies have very high mortality rates, as is fitting for being in very poor shape, burdened by the damage of aging, but those very high rates appear to plateau. Over the past fifteen years, various analyses have suggested and then refuted that such a plateau exists in humans. Again we come back to the point that the data for very advanced ages isn’t all that great, and so there tends to be a great deal of debate. At present, the balance of evidence and argument suggests that, for our species at least, mortality rates do keep increasing past the age of 110.

Are We Approaching a Biological Limit to Human Longevity?

Until recently human longevity records continued to grow in history, with no indication of approaching a hypothetical longevity limit. Also, earlier studies found that age-specific death rates cease to increase at advanced ages (mortality plateau) suggesting the absence of fixed limit to longevity too. In this study we re-examine both claims with more recent and reliable data on supercentenarians (persons aged 110 years and over).

We found that despite a dramatic historical increase in the number of supercentenarians, further growth of human longevity records in subsequent birth cohorts slowed down significantly and almost stopped for those born after 1879. We also found an exponential acceleration of age-specific death rates for persons older than 113 years in more recent data. Slowing down the historical progress in maximum reported age at death and accelerated growth of age-specific death rates after age 113 years in recent birth cohorts may indicate the need for more conservative estimates for future longevity records unless a scientific breakthrough in delaying aging would happen.

Many gerontologists are now more conservative regarding the future growth of longevity, citing results confirm that further growth of maximum lifespan for humans becomes an increasingly difficult task. Still there are reasons for cautious optimism here. Systematic analysis of human mortality throughout the 20th century revealed that, once a particular cause of death is accounted for, there is a proportional increase in both median age of death and maximum life span. So the authors of this study believe that application of aging-focused interventions could result in a continued increase not only in the median, but in maximal life span in humans as well.

Further research is needed to overcome obvious limitations of our study by addressing remaining concerns about data quality and representativeness, as well as increasing sample sizes. Still the data used in our study are the best available data so far, and their analysis suggests that there may be a provisional limit to human life in our current state of biomedical knowledge.

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Both Extracellular Vesicles and Secreted Proteins can Spread Cellular Senescence

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The accumulation of senescent cells with age is one of the root causes of aging. Senescent cells never amount to more than a few percent of all cells, even in late life, but they secrete a mix of extracellular vesicles and various proteins that is inflammatory and disruptive to tissue function. This is known as the senescence-associated secretory phenotype, or SASP. Since senescent cells inflect harm through signaling, it doesn’t take many such cells to act as a contributing cause of age-related disease and organ dysfunction.

The research community is nowadays fully invested in the concept that senescent cells are a meaningful cause of aging. This is a comparatively recent development, despite the fact that the evidence was sizable and evident for several decades. It took a great deal of hard work, advocacy, and philanthropy in order to bring about this change; the medical research and development communities had essentially relinquished their responsibilities in the matter of aging. Now, however, there is a great deal of funding for research groups interested in the biochemistry of senescent cells.

While most clinical development is focused on selective destruction of senescent cells as a way to reverse their contribution to the aging process, and this seems the best path forward, there is nonetheless a sizable faction in the research community whose members are more interested in modulating the bad behavior of senescent cells. This largely means interfering the generation or consequences of the SASP in some way. One of the consequences of SASP signaling is that nearby cells are encouraged to become senescent themselves. In today’s open access paper, the authors report on their investigation of the mechanisms involved in this behavior.

Small Extracellular Vesicles Are Key Regulators of Non-cell Autonomous Intercellular Communication in Senescence via the Interferon Protein IFITM3

The establishment of cellular senescence is categorized by a stable cell-cycle arrest and the capacity to modify the microenvironment through a particular secretome called SASP (senescence-associated secretory phenotype). The activation of senescence is a response to different cellular stresses to prevent the propagation of damaged cells and has been shown to occur in vitro and in vivo. In fact, an enrichment in the number of senescent cells has been observed in vivo during both biological and pathological processes such as development, cancer, fibrosis, and wound healing.

The SASP controls its surroundings by reinforcing senescence in an autocrine (cell autonomous) and paracrine (non-cell autonomous) manner, by recruiting immune cells to eliminate senescent cells and by inducing a stem cell-like phenotype in damaged cells. The SASP provides the necessary balance to restore tissue homeostasis when it has been compromised. Paradoxically, the SASP can also contribute to the enhancement of tissue damage and the induction of inflammation and cancer proliferation. Overall, the mechanisms behind the pleiotropic activities of the SASP in different contexts are not well understood.

Most studies in vitro and in vivo have attributed the diverse functions of the SASP to individual protein components such as interleukin-6 (IL-6) or IL-8 to reinforce autocrine senescence or transforming growth factor β (TGF-β) as the main mediator of paracrine senescence or to a dynamic SASP with a switch between TGF-β and IL-6 as predominant individual components. However, it is still unclear how these diverse SASP components regulate senescence. In fact, inhibition of the SASP by blocking the mammalian target of rapamycin (mTOR) only partially prevents paracrine senescence, suggesting that alternative mechanisms may exist.

Exosomes are small extracellular vesicles (sEVs) (30-120 nm) of endocytic origin, whereas microvesicles are formed by the shedding of the plasma membrane. Exosomes and microvesicles are secreted by all cell types and found in most bodily fluids. Although some studies have found an increase in the number of EVs released during senescence, very little is known regarding the role that EVs play as SASP mediators in the senescent microenvironment.

Here, we show that both the soluble and sEV fractions of the SASP transmit paracrine senescence. The analysis of individual cells internalizing sEVs using a reporter system shows a positive correlation between the uptake of sEVs and paracrine senescence. sEV protein characterization by mass spectrometry (MS) followed by a functional small interfering RNA (siRNA) screen identify the interferon (IFN)-induced transmembrane protein 3 (IFITM3) within sEVs as partially responsible for transmitting senescence to normal cells. It is interesting that elderly human donors release more sEVs and that the sEVs found in plasma show higher protein levels of IFITM3 in 60% of the elderly donors. Although it may be tempting to speculate that IFITM3 within sEVs could be involved in aging, a larger cohort of young and elderly patients would be needed.

In conclusion, we show here that sEVs are responsible for mediating paracrine senescence and speculate that they could be involved in inducing bystander senescence during therapy-induced senescence or aging. In fact, when compared to soluble factors, sEVs have different biophysical and biochemical properties as they have a longer lifespan than do soluble factors and they are more resistant to protease degradation. The idea that blocking sEV secretion could be a potential therapeutic approach to alleviate senescence “spreading” during chemotherapy-induced senescence or in aging tissues presents itself as a very attractive tool for the future.

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Reviewing Resistance Training as an Intervention to Reduce Chronic Disease Risk

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A sizable body of evidence points to the ability of resistance training undertaken in later life to reduce the risk of suffering age-related disease, and to improve the prognosis for existing diseases. In a glass half empty sort of a viewpoint, we might take this to mean that next to nobody puts in the effort necessary to maintain the body in an optimal state of health. A surprisingly sizable fraction of the declines in strength and fitness observed in the wealthier parts of the world are actually self-inflicted, not an inevitable consequence of aging. This is particularly apparent in comparisons with hunter-gatherer populations, where exercise and fitness persist into late middle age, and the declines that are inevitable are lessened.

The progressive decline of skeletal muscle mass and strength with aging is collectively referred to as sarcopenia, and is prognostic for mobility disability and chronic disease risk. Regular physical activity (defined here as any bodily movement produced by the contraction of skeletal muscle that increases energy expenditure) and exercise (physical activity that is planned, structured, and repetitive) are cornerstones in the primary prevention of chronic diseases and also for mitigating risk of mobility disability in older persons.

Resistance exercise (RE) and aerobic exercise (AE) are modalities of exercise that are traditionally conceptualized as existing on opposite ends of an exercise continuum in terms of the phenotypes they lead to. A common misconception is that RE training (RET) and AE training (AET) also result in separate health benefits, but we propose this is an artifact of the greater volume of data that currently exists for AET as opposed to RET. Currently, most physical activity guidelines advise, as their primary message, that older adults should perform at least 150 min of moderate-to-vigorous or 75 min of vigorous AET weekly for the reduction of chronic disease risk and maintenance of functional abilities. However, there is an emerging body of evidence to suggest that RET can be as effective as AET in reducing chronic disease risk and is particularly potent for maintaining mobility in older adults.

It may be that RET is more effective than AET in some regards; the converse is likely also true. We posit that the perceived divergent exercise mode-dependent health benefits of AET and RET are likely small in most cases. In this short review, our aim is to examine evidence of associations between the performance of RET and chronic health disease risk (mobility disability, type 2 diabetes, cardiovascular disease, cancer). We also postulate on how RET may be influencing chronic disease risk and how it is a critical component for healthy aging. Accumulating evidence points to RET as a potent and robust preventive strategy against a number of chronic diseases traditionally associated with the performance of AET, but evidence favors RET as a potent countermeasure against declines in mobility. On the basis of this review we propose that the promotion of RET should assume a more prominent position in exercise guidelines particularly for older persons.


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Quiescence of Stem Cells in Aging as a Double Edged Sword

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Stem cells spend much of their time in the quiescent stage of the cell cycle, resting without replication in a state of lower metabolic activity. The open access review paper here is an interesting look at why quiescence is both helpful and problematic in the context of the contribution of stem cell dysfunction to aging and age-related disease. The purpose of stem cells is to support the surrounding tissue by providing a supply of daughter somatic cells to replace losses and repair damage. Stem cell populations decline in this activity with aging, due to a mix of cellular damage, a fall in numbers, and increasing quiescence. To the degree that the latter of these issues is dominant, it should be possible to find ways to push stem cells back into greater activity. Indeed, many present approaches to regenerative medicine aim at this goal.

The quiescence stage of stem cells has beneficial and adverse effects on stem cell aging. Stem cell quiescence delays stem cell aging by reducing DNA replication, metabolic activity, gene transcription, and mRNA translation, since all of these activities are accompanied by induction of molecular damage. Stem cell quiescence comes at the cost of impaired expression of repair factors in quiescence and increased vulnerability in response to stem cell activation requiring the concerted and faithful activation of multiple molecular circuits controlling biosynthetic processes, repair, and metabolic activity.

Aging-associated increases in stem cell-intrinsic accumulation of molecular damage as well as stem cell-extrinsic alterations (e.g., chronic inflammation, niche cell defects) contribute to the deregulation of quiescence maintenance and increasing vulnerability during exit from quiescence. Epigenetic alterations occur during aging in quiescent and activated stem cells and lead to aberrant expression of developmental genes resulting in alterations of quiescence maintenance, self-renewal, and differentiation.

In conclusion, quiescence protects stem cells against molecular damage but comes at the cost of aging-associated failure in the correct regulation of quiescence maintenance and exit. Activation of quiescent stem cells – an essential process for organ homeostasis/regeneration – requires concerted and faithful regulation of multiple molecular circuits controlling biosynthetic processes, repair mechanisms, and metabolic activity. Thus, while protecting stem cell maintenance, quiescence comes at the cost of vulnerability during the process of stem cell activation.


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Telomere Dynamics with Age are Very Different Between Mammalian Species

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Telomeres are caps of repeated DNA sequences at the ends of chromosomes. They shorten with each cell division, a part of the mechanism that ensures somatic cells can only replicate a limited number of times. Telomerase acts to lengthen telomeres, and in humans telomerase is only active in stem cells. Thus our cells exist in a two-tier system, in which only tiny populations of privileged stem cells are permitted unrestricted replication, while the vast majority of somatic cells are limited. Matters are similar across all higher animals, and this state of affairs likely evolved because it keeps cancer to a low enough level, and pushed off far enough into late life, for allow for evolutionary success.

A lot of ink has been spilled on the topic of telomere length because, statistically across large populations, average telomere length and proportion of short telomeres tends to decrease with advancing age. Given that stem cell activity declines with age, this is most likely a reflection of a lower pace of creation of new somatic cells with long telomeres. The human data is complicated by the fact that telomere length is most commonly measured in immune cells from a blood sample, and is thus a very dynamic measure influenced by the day to day reactions of the immune system. In individuals, there isn’t much anyone can do with measures of telomere length, given that it is so variable over time and between people of similar health and age: it is a terrible biomarker for any practical purpose.

Further, can we actually use anything that we learn about telomere dynamics in other species? It is well known that mouse telomere dynamics and telomerase expression are quite different from that of humans. This might make us suspect that positive results from telomerase gene therapies in mice, where life span is extended and health improved, without raising the risk of cancer, may not hold up in humans. There is no particular reason why increased cancer risk through putting damaged cells back to work will be balanced in the same way by improved tissue function and improved immune function, from species to species. The research and development community will find out in the years ahead by trying telomerase gene therapies in primates and then humans.

I feel that the open access paper here adds to doubts about the value that the research community can extract from a study of telomeres and telomerase in other mammalian species, though the researchers don’t present it in that way. If various short and long lived mammals can have such a range of telomere dynamics, what are we supposed to make of the data resulting from animal studies of any therapeutic approach to targeting telomeres?

Telomeres and Longevity: A Cause or an Effect?

Since telomere dynamics were found to be better predictors of survival and mortality than chronological age in wild populations, many cross-sectional and longitudinal studies have been conducted on different organisms with variations in maximum life span investigating the relationship between chronologic age and telomere shortening. Yet, some studies have reported a lack of telomere shortening with age or even an increase in telomere length in organisms with exceptional longevity. Therefore, studying telomere dynamics in long-lived organisms is of particular importance since they may have developed mechanisms that actively postpone senescence and promote effective defenses against the deteriorating effects of aging processes.

The naked mole-rat (Hetercephallus glabers/NMR) and the blind mole-rat (Spalax ehrenbergi) are both considered excellent models for studying aging. They both exhibit extraordinary longevity with a maximum lifespan of approximately 30 years in NMRs (10 times longer than any other rodent of the same size) and 20 years in captivity for Spalax. They exhibit lifelong maintenance of superior anti-aging mechanisms leading to unchanged physiological functions and negligible senescence. Moreover, both of these mole-rats live in a presumably relatively stressful environment due to their subterranean lifestyle where they experience darkness, low oxygen and high carbon dioxide concentrations. Despite all these common features, NMRs and Spalax belong to different families; they are different in size and have different social lifestyles.

Whether telomere length is a “biological thermometer” that reflects the biological state at a certain point in life or a biomarker that can influence biological conditions, delay senescence, and promote longevity is still an ongoing debate. In the current study, we aimed to investigate the relationship between telomere length and age in NMRs and Spalax. We tested blood telomeres in NMRs and three different tissues in Spalax and compared each one with a short-lived animal of their size.

While blood telomere length of the naked mole-rat (NMR) did not shorten with age but rather showed a mild elongation, telomere length in three tissues tested in the Spalax declined with age, just like in short-lived rodents. These findings in the NMR suggest an age buffering mechanism, while in Spalax tissues the shortening of the telomeres are in spite of its extreme longevity traits. Therefore, using long-lived species as models for understanding the role of telomeres in longevity is of great importance since they may encompass mechanisms that postpone aging.

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More Supporting Evidence for Pancreatic Fat to be the Cause of Type 2 Diabetes

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Type 2 diabetes is, for the vast majority of patients, a condition caused by being significantly overweight. Age does has an influence on the risk of being overweight leading to metabolic syndrome and then type 2 diabetes; it is reasonable to say that type 2 diabetes is an age-related condition. In essence, the younger you are, the more fat tissue it requires to push your metabolism over the red line. A few years back, researchers demonstrated that it is specifically fat in the pancreas that causes type 2 diabetes. Of course the only way to put that fat into the pancreas in the normal course of affairs is to become very overweight, creating fat tissue around all of the organs important to metabolism, and negatively influencing their function.

Now, a few years down the line, and as a result of the rapid growth of interest in senescent cells as a cause of aging and age-related disease, we know that (a) excess visceral fat tissue produces chronic inflammation through, among other mechanisms, a more rapid generation of senescent cells, and (b) much of the detrimental effects of type 2 diabetes appear to be mediated by the presence of senescent cells in the pancreas. Treating animals with senolytic drugs reverses many of the effects of the condition. So this all ties together quite nicely as a view of how and why type 2 diabetes occurs. Given that cellular senescence becomes more prevalent in older individuals, that also fits.

While I’m sure that there will be, soon enough, tremendous interest in senolytic therapies from the sizable overweight and diabetic population of the wealthier portions of the world, it remains the case that the most reliable approach to reversing type 2 diabetes, even at the later stages, is to lose the excess weight. Excess visceral fat tissue is required to maintain that harmful fat in the pancreas, and losing weight removes it. Fasting and very low calorie diets also seem quite effective at removing fat from the pancreas, perhaps more rapidly than would occur just by losing the visceral fat tissue via the usual, slow calorie deficit method, based on human trials of this approach.

Promising approach: Prevent diabetes with intermittent fasting

Fatty liver has been thoroughly investigated as a known and frequently occurring disease. However, little is known about excess weight-induced fat accumulation in the pancreas and its effects on the onset of type 2 diabetes. Researchers have now found that overweight mice prone to diabetes have a high accumulation of fat cells in the pancreas. Mice resistant to diabetes due to their genetic make-up despite excess weight had hardly any fat in the pancreas, but instead had fat deposits in the liver.

The team of scientists divided the overweight animals, which were prone to diabetes, into two groups: The first group was allowed to eat ad libitum – as much as they wanted whenever they wanted. The second group underwent an intermittent fasting regimen: one day the rodents received unlimited chow and the next day they were not fed at all. After five weeks, the researchers observed differences in the pancreas of the mice: Fat cells accumulated in group one. The animals in group two, on the other hand, had hardly any fat deposits in the pancreas.

In order to find out how fat cells might impair the function of the pancreas, researchers isolated adipocyte precursor cells from the pancreas of mice for the first time and allowed them to differentiate into mature fat cells. If the mature fat cells were subsequently cultivated together with the Langerhans islets of the pancreas, the beta cells of the islets increasingly secreted insulin. “We suspect that the increased secretion of insulin causes the Langerhans islets of diabetes-prone animals to deplete more quickly and, after some time, to cease functioning completely. In this way, fat accumulation in the pancreas could contribute to the development of type 2 diabetes.”

Pancreatic adipocytes mediate hypersecretion of insulin in diabetes-susceptible mice

Ectopic fat accumulation in the pancreas in response to obesity and its implication on the onset of type 2 diabetes remain poorly understood. Intermittent fasting (IF) is known to improve glucose homeostasis and insulin resistance. However, the effects of IF on fat in the pancreas and β-cell function remain largely unknown. Our aim was to evaluate the impact of IF on pancreatic fat accumulation and its effects on islet function.

New Zealand Obese (NZO) mice were fed a high-fat diet ad libitum (NZO-AL) or fasted every other day (intermittent fasting, NZO-IF) and pancreatic fat accumulation, glucose homoeostasis, insulin sensitivity, and islet function were determined and compared to ad libitum-fed B6.V-Lepob/ob (ob/ob) mice. To investigate the crosstalk of pancreatic adipocytes and islets, co-culture experiments were performed.

NZO-IF mice displayed better glucose homeostasis and lower fat accumulation in both the pancreas (-32%) and the liver (-35%) than NZO-AL mice. Ob/ob animals were insulin-resistant and had low fat in the pancreas but high fat in the liver. NZO-AL mice showed increased fat accumulation in both organs and exhibited an impaired islet function. Co-culture experiments demonstrated that pancreatic adipocytes induced a hypersecretion of insulin and released higher levels of free fatty acids than adipocytes of inguinal white adipose tissue.

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Statins double diabetes rates

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Statins are a type of medication prescribed to lower cholesterol levels. They work by blocking an enzyme in the liver your body uses to make cholesterol.1 Although vilified for many years as causing heart attacks and stroke,2 your body makes cholesterol as it is needed to produce hormones, build cell membranes and produce substances used to digest food.3

Cholesterol is found in foods from animals, such as dairy products and meats.4 Your body makes the fatty substance cholesterol, but it cannot travel in the bloodstream alone.5 The body encases small particles of cholesterol inside protein particles that are able to mix easily with the blood. These are called lipoproteins and they’re responsible for transporting cholesterol.6

One of the main types of lipoproteins is high-density lipoprotein (HDL), sometimes called the “good” cholesterol as its job is to collect cholesterol and deliver it to your liver where it’s removed.7

Low density lipoprotein (LDL) and very low-density lipoprotein (VLDL) are often referred to as “bad.”8 It’s important to remember that only 20% of the cholesterol in your body is acquired from the food you eat, while the rest is made by your body.9

Prescriptions for statins are written to reduce the levels of cholesterol made by the body.10 However, since your body is so complex, changing one factor often results in unintended events, sometimes called side effects or adverse reactions.11 As suggested by one study, one adverse reaction from statin drugs may be doubling your risk of Type 2 diabetes.12

Risk of diabetes doubles with cholesterol medication

Past studies have demonstrated that statins increase the risk of diabetes.13 A new study led by a graduate researcher at The Ohio State University14 explored this link in research published in Diabetes Metabolism Research and Reviews. The study was a retrospective evaluation of medical records using employees and spouses from a private insurance plan.

Yearly biometric screening, health surveys, medical claims and pharmacy data were gathered from 2011 through 2014.15 Individuals who had indications for statin use, or who had a previous cardiovascular event, were enrolled. Adults who had Type 2 diabetes before the study or who acquired it in the first 90 days were excluded.

Records were classified as belonging to a statin user if they had two or more prescriptions filled, but individuals using statins before January 2011 or within the first 90 days of enrollment in the insurance were excluded. Data were collected from 755 individuals using statins and 3,928 who were not.16

After accounting for factors such as age, gender, ethnicity, education and body mass index, the researchers found those who used statins during the study were two times as likely to be diagnosed with diabetes than those who did not take statin medications.17

Interestingly, individuals who used statin drugs longer than two years experienced an increased risk of more than three times as likely to get the disease.18 The data also indicated that individuals taking statin medications had a 6.5% increased risk of high blood sugar as measured by hemoglobin A1c values.

The hemoglobin A1c blood test is an average level of blood sugar measuring the past 60 to 90 days.19 The test measures how much sugar is bound to hemoglobin on red blood cells. Since red blood cells live for up to 90 days, the test is an average of your blood glucose level during this time.

Take one medicine for the side effects of another, and so on

In 2012, the FDA20 approved changes to labels on statin medications to provide information on adverse events, including reports of increased blood sugar and higher A1c testing. Other side effects listed on the label included cognitive effects such as memory loss and confusion.

While there had been reports of rare but serious liver conditions in those taking statin medications,21 in the same announcement, the FDA22 removed the need for routine monitoring of liver enzymes and recommended they should be performed before starting therapy and then as clinically necessary. Since severe injury was rare, they concluded routine monitoring would not be effective.

The NHS, National Health Services from England, recommends23 statins should not be used in those with severe liver disease since they affect your liver and are “more likely to cause serious problems if you already have a severely damaged liver.”

In 2014,24 one team of researchers discovered adding Glyburide to a statin regimen suppressed the immune response they believed was responsible for the development of Type 2 diabetes. The team led by Jonathan Schertzer, Ph.D., from McMaster University, believed this finding may lead to a next generation of statins. As reported in a press release:25

“Recently, an increased risk of diabetes has been added to the warning label for statin use. This was perplexing to us because if you are improving your metabolic profile with statins you should actually be decreasing the incidence of diabetes with these drugs, yet, the opposite happened.

We found that statins activated a very specific immune response, which stopped insulin from doing its job properly. So we connected the dots and found that combining statins with another drug on top of it, Glyburide, suppressed this side effect.”

In other words, to offset a significant adverse event from one drug, the team recommended the addition of a second drug, which comes with an additional list of side effects including vasculitis, hyponatremia (low blood sodium associated with confusion, seizures and muscle weakness),26 alopecia and liver damage.27

One journalist for commented on this turn of events, saying: “However, as glyburide stimulates insulin production, using a type 2 diabetes drug to prevent type 2 diabetes seems a peculiar treatment.”28

Statins trigger high number of side effects

Statin medications deplete your body of coenzyme Q10 (CoQ10), which may account for some of the devastating long-term results. It was strongly suggested29 the FDA add a black box warning to statin medications to advise patients and physicians about this, but in 2014 the FDA decided against it.30

The reduction in CoQ10 may be responsible for an increased risk of acute heart failure31 and atherosclerosis, as reported in a 2015 scientific investigation.32 The study addressed physiological mechanisms in the reduction of CoQ10, including the inhibition of the synthesis of vitamin K2 necessary to protect against arterial calcification.

A reduction in vitamin K2 may contribute to osteoporosis,33heart disease,34 brain disease35 and inappropriate calcification.36 Statins have also been associated with an increased risk of neurodegenerative diseases,37 cataracts,38 cancer.39,40 and musculoskeletal disorders.41

In one study,42 a research team evaluated the use of statins in patients with terminal illnesses who had a high likelihood of dying within one year. They found those who stopped taking statins had a mean survival of 39 more days than those who continued to take statins — 229 days without statins and 190 days with statins.

Although the FDA calls liver complications rare, one physician’s43 search of MedWatch, the FDA’s Adverse Event Reporting Program, found 5,405 individuals reporting hepatitis or liver function abnormalities associated with just two statin medications between 2006 and 2013.

Effectiveness of statins lower than publicized

How effective a medication may or may not be is expressed as relative risk or absolute risk.44 If the type of risk is not identified it may be difficult to determine whether taking action would affect you.

For instance, if a medication under investigation to prevent prostate cancer enrolls 200 men and splits them into two equal groups, one is likely to receive a placebo and the other is likely to receive the experimental drug. In the placebo group, two men may develop prostate cancer; in the treatment group, perhaps only one man develops it. When compared, the researchers find there’s a 50% reduction in relative risk.

Relative risk is determined by comparing the number between two groups. One man developed it in the treatment group and two in the control group. Since one is half of 2, there’s a 50% reduction in the development of the disease. The absolute risk is far smaller.

The risk of developing prostate cancer in the control group was 2%, since two out of 100 developed prostate cancer, but in the treatment group it was 1%. This means there’s a 1% absolute risk of developing prostate cancer with the medication as compared to 2%. Your absolute risk is not 50% less but rather just 1% less when taking the medication.

Knowing the difference between relative risk and absolute risk is necessary when balancing the benefits of statin medications against the side effects and adverse events. If you are in a position of needing to decide to use statin medications, it’s important to note the relative reduction in risk of a major cardiac event while using statins was between 20% and 25%.

In the case of having to decide whether the potential benefits of statins are worth the known risks, for example, it’s important to consider a report from 2016. In an Expert Analysis article, it was noted that a meta-analysis45 of 27 randomized trials revealed that “[F]or every ~40mg/dL LDL-C reduction with statin therapy, the relative risk of major adverse events is reduced by ~20-25%, and all-cause mortality is reduced by 10%.”

While another study found a similar relative risk, the actual difference in rates of coronary death in the population was 9% in the placebo group and 6.7% in those who were treated with statins.46

Researchers therefore found the difference between the treated and untreated groups was a mere 2.3% and not the inflated relative risk of 28%. They wrote that while the reduction in relative risk appears impressive to some readers, this form of data presentation is misleading.47

Simple strategies to normalize your cholesterol levels

Before becoming concerned about your cholesterol levels, it’s important to evaluate whether you really need a statin drug to reduce your risk of a cardiovascular event. Updated guidelines published by the American Heart Association and the American College of Cardiology are based on a personalized risk assessment.48

However, the U.S. Department of Health and Human Services critically evaluates those with cholesterol levels over 200 milligrams per deciliter.49 I believe this total cholesterol measurement has little benefit in evaluating your risk for heart disease unless the number is over 300.

In some instances, high cholesterol may indicate a problem, provided it’s your LDL or triglycerides and you have low HDL. A better evaluation of your risk of heart disease are these two ratios in combination with other lifestyle factors, such as your iron level and diet.

  • HDL/Cholesterol ratio — Divide your HDL level by your cholesterol. This ratio should ideally be above 24 percent.
  • Triglyceride/HDL ratio — Divide your triglyceride level by your HDL. This ratio should ideally be below 2. Data demonstrate a ratio greater than four is a powerful predictor of coronary artery disease.50

You have control over your health and may protect your heart and lower your risk of heart disease by following suggestions affecting your lifestyle and exposure to environmental toxins. In my article, “Cholesterol managers want to double statin prescriptions,” I share a list of suggestions to help minimize your toxic exposure and improve your body’s ability to maintain good heart health.

Additionally, in my article “Nearly half of American adults have cardiovascular disease,” I summarize additional strategies you may use to improve microcirculation in your heart. I also talk about mitochondrial function and insulin resistance, which are related to strong heart health.

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OncoSenX Raises $3 Million to Adapt the Oisin Biotechnologies Platform to Cancer

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Oisin Biotechnologies uses a form of programmable suicide gene therapy to target senescent cells for destruction. The therapy can be triggered by expression of specific genes inside a cell, and so beyond senescent cells there is a long, long list of possibly harmful cell populations in aging and disease that it would be beneficial to remove. The obvious first choice is cancerous cells with a mutation in one of the common cancer suppressor genes, such that the gene is expressed but not helping. Thus Oisin Biotechnologies spun out OncoSenX last year. The company is moving forward towards trials, and recently raised a seed round to fund the work of the next few years.

OncoSenX, Inc., a late preclinical-stage company developing therapeutics to kill cancer cells based on their genetics, today announced it has raised $3 million in pre-seed funding to advance its pipeline. “These funds will allow us to accelerate the preclinical research necessary for us to begin phase 1 clinical development. We believe our non-viral gene therapy for solid tumors represents the first in a new class of cancer therapeutics. The OncoSenX team is diligently working to bring this new approach into the clinic for the benefit of a global oncology community clearly in need of new options.”

OncoSenX is developing a highly selective tumor-killing platform with two main components: a proprietary lipid nanoparticle (LNP) for cellular delivery and a highly selective DNA payload. The LNP is designed to deliver its non-integrating DNA payload to solid tumors, while an engineered promoter drives expression of a potent, inducible death protein only in the target cell population. The goal is to precisely target cell populations based on their genetic activity without harming nearby cells. The platform can be effectively programmed to implement logic gates (IF/OR/AND) to provide selectivity to any target cell based on its genetics.

“Our preclinical studies suggest the OncoSenX approach has the potential to precisely kill cancer cells based on the mutations they harbor. If substantiated in the clinic, the platform could deliver reduced toxicity and improved tolerability over conventional chemotherapy, with the potential for superior targeting over biologics or even CAR-T therapy.”


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Applying Bacterial Homing Strategies to Target Stem Cells to Heart Tissue

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Most classes of therapy benefit from some form of targeting or selectivity, helping to direct them to the tissue of interest, and away from other places where they might cause side-effects. Cells are difficult to work with, but they are also much more capable of selective targeting, since they can migrate. Many types of cell reliably find their way from one part of the body to another in the course of their functions, but where no suitable mechanism exists in human biochemistry, it is sometimes possible to look elsewhere. Here, researchers adapt a bacterial targeting system and apply it to the stem cells that might be used in regenerative therapies for damaged heart tissue.

To date, trials using stem cells, which are taken and grown from the patient or donor and injected into the patient’s heart to regenerate damaged tissue, have produced promising results. However, while these next generation cell therapies are on the horizon, significant challenges associated with the distribution of the stem cells have remained. High blood flow in the heart combined with various ’tissue sinks’, that circulating cells come into contact with, means the majority of the stem cells end up in the lungs and spleen.

“We know that some bacterial cells contain properties that enable them to detect and ‘home’ to diseased tissue. For example, the oral bacterial found in our mouths can occasionally cause strep throat. If it enters the blood stream it can ‘home’ to damaged tissue in the heart causing infective endocarditis. Our aim was to replicate the homing ability of bacteria cells and apply it to stem cells.” The team developed the technology by looking at how bacterial cells use a protein called an adhesin to ‘home’ to heart tissue. Using this theory, the researchers were able to produce an artificial cell membrane binding version of the adhesin that could be ‘painted’ on the outside of the stem cells. In an animal model, the team were able to demonstrate that this new cell modification technique worked by directing stem cells to the heart in a mouse.

“Our findings demonstrate that the cardiac homing properties of infectious bacteria can be transferred to human stem cells. Significantly, we show in a mouse model that the designer adhesin protein spontaneously inserts into the plasma membrane of the stem cells with no cytotoxity, and then directs the modified cells to the heart after transplant. To our knowledge, this is the first time that the targeting properties of infectious bacteria have been transferred to mammalian cells.”


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Rate of Telomere Shortening Correlates with Species Average Life Span

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Researchers here report on data showing a correlation between species life span and pace of telomere shortening. Telomeres are the repeated DNA sequences at the ends of chromosomes. A little is lost with each cell division, during replication of DNA, and cells with very short telomeres become senescent or self-destruct. This is how the vast majority of cells in the body are limited in their replicative capacity, in order to lower the risk of damaged cells becoming cancerous to an evolutionarily acceptable level. Not a personally acceptable level, of course.

With age, average telomere length tends to shorten in most species, and this is most likely a reflection of loss of stem cell function. Stem cells maintain long telomeres via use of telomerase, and thus the daughter somatic cells they provide to support surrounding tissue also have long telomeres. Given fewer such daughter cells, average telomere length diminishes, along with tissue function – but that loss of telomere length isn’t the cause of loss of tissue function.

Nonetheless, telomerase gene therapy extends life in mice, most likely by inducing damaged cells to greater activity in tissue maintenance. Since the immune system is most likely improved as well, this treatment doesn’t lead to a greater incidence of cancer, which would be the usual outcome of making damage cells do more work. This hypothesis on what takes place in telomerase gene therapy is still not a suggestion that telomere shortening is a cause of aging. In this view telomerase gene therapy is conceptually similar to stem cell therapies or signaling therapies that increase native cell activity without repairing the underlying damage that caused the decline. As noted in the publicity materials, this particular research group is generally in favor of the opposite viewpoint, that telomere shortening is an important causative mechanism of aging, rather than a largely downstream reflection of other issues.

Researchers discover that the rate of telomere shortening predicts species lifespan

After analyzing nine species of mammals and birds, researchers found a very clear relationship between the lifespan of these species and the shortening rate of their telomeres, the structures that protect the chromosomes and the genes they contain. The fit is better when using the average lifespan of the species – 79 years in the case of humans – rather than the maximum lifespan -the 122 documented years lived by the Frenchwoman Jeanne Calment.

Until now, however, no relationship had been found between telomere length and lifespan of each species. There are species with very long telomeres that are short-lived and vice versa. The researchers decided not to compare the absolute length of the telomeres, but rather their rate of shortening. It is the first large-scale study that compares this highly variable parameter between species: human telomeres lose on average about 70 base pairs – the building blocks of the genetic material – per year, whereas those of mice lose about 7,000 base pairs per year.

“This study confirms that telomeres play an important role in aging. There are people who are not convinced, and they say that for example mice live two years and have very long telomeres, while humans live much longer and have short telomeres; but we have shown that the important thing is not the initial length but the rate of shortening and this parameter predicts the longevity of a species with a high degree of precision.”

Telomere shortening rate predicts species life span

Telomere shortening to a critical length can trigger aging and shorter life spans in mice and humans by a mechanism that involves induction of a persistent DNA damage response at chromosome ends and loss of cellular viability. However, whether telomere length is a universal determinant of species longevity is not known. To determine whether telomere shortening can be a single parameter to predict species longevities, here we measured in parallel the telomere length of a wide variety of species (birds and mammals) with very different life spans and body sizes, including mouse (Mus musculus), goat (Capra hircus), Audouin’s gull (Larus audouinii), reindeer (Rangifer tarandus), griffon vulture (Gyps fulvus), bottlenose dolphin (Tursiops truncatus), American flamingo (Phoenicopterus ruber), and Sumatran elephant (Elephas maximus sumatranus).

We found that the telomere shortening rate, but not the initial telomere length alone, is a powerful predictor of species life span. These results support the notion that critical telomere shortening and the consequent onset of telomeric DNA damage and cellular senescence are a general determinant of species life span.

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