How will you die? The four deadly killers

Ever since science effectively cured infectious disease through antibiotics, vaccinations and the like, there has been a distinct shift in what kills humans to the four deadly killers, which are considered ‘age related diseases’. These are — cardiovascular disease, neurodegenerative disease, metabolic disease and cancer. If you manage to escape the most likely causes of death as a young person, which are largely accidental accidental death (mostly car accidents), homicide or mental illness related (suicide) — then it is most likely that one of those four deadly killers will end your life.

But here’s the good news — there’s a growing body of immediately actionable longevity technologies that you can engage with to offset your risk of dying of these diseases. In a series of posts on the topic, I’m going to cover a few key resources at your disposal for minimising your risk for each of these four categories. First-up, cardiovascular disease.

Deadly Killer #1 — Cardiovascular disease

Heart attack, stroke, thrombosis, heart failure — the chances are overwhelming that you have lost someone important to you in your life to one of these causes. It is often seemingly sudden, but in most cases, the acute cause of death by cardiovascular disease has been brewing for a very long time — decades even.

The term ‘cardiovascular’ encompasses disease of both the heart and blood vessels, which is driven by the build up and eventual displacement of plaque that accumulated in the arterial wall in a process called ‘atherosclerosis’.

It’s not my role here to explain all of the mechanisms of this disease. Instead, I want to focus on four actionable tools you can work with your doctor to obtain access to, which will help you assess your risk profile and detect any elevated risk of an acute event (e.g. heart attack, stroke) at an early, treatable stage:

1. Test your ApoB (“A-PO-B”)

Stop using your LDL-C as your primary risk assessment tool (The “LDL” value too commonly called the “bad” cholesterol), and start tracking your ApoB. ApoB is a particular type of molecule attached to the types of lipoproteins carried by your LDL (and VLDL) that are the most likely to enter the arterial wall and lead to plaque formation. You need to know *how many* of these atherogenic particles you have present in a given volume of you blood — this drives your risk. Your ApoB value is influenced by diet and lifestyle and can be controlled with pharmaceutical intervention and possibly through certain forms of supplementation.

Learn more about ApoB at Healthline.

2. Do you have elevated Lpa (”L-P-little-A”)?

Lpa is another cardiovascular disease bad guy that may be in your bloodstream. Lipoprotein-a is a particle which carries cholesterol, fats and proteins and is made by your body, and how much of it you make is inherited. Elevated levels of Lpa increase your risk of a heart attack or stroke as they are known to cause atherosclerosis. You certainly need to know if you carry the genetic risk factor, and the earlier the better (i.e. get this test done as early as possible)! Levels of Lpa don’t change much over one’s lifetime, so testing it once is enough in most cases! Know your Lpa status, and better know your risk, and whether or not you should modify your diet, lifestyle and treatment options.

Learn more about Lpa from the lipoprotein-a foundation

3. Know your Coronary Artery Calcium scan score

Coronary artery calcium (CAC) scans are created by using computed tomography (CT) scans, which are a type of X-ray scan, to detect the presence and quantity of coronary artery calcification (the warning signs of atherosclerosis).

A CAC test reveals both the location and quantity of calcium located in three of the main coronary arteries. The scan provides a score which represents your risk. The lower the better! This score will change over time, and is known to increase with age, so it is important to record it regularly (in a manner that balances the downsides of the X-ray radiation — ask your doctor what’s best for you). Atherosclerosis is a disease of ageing, and that means your risk is increasing over time. If you are aged 50 or above and have never had one — work with your doctor to get one performed.

4. Track your inflammation with C-Reactive Protein (CRP)

At its roots, atherosclerosis is known to be intimately connected with inflammation. In fact, it is often damage to the arterial wall that attracts the formation of plaque in the first place. This damage occurs over time, and is known to be increasingly likely with high blood pressure and high blood glucose levels. CRP is a very common and relatively low cost blood test that can be easily ordered up by your doctor, and should be tested annually at the very least. High levels of CRP are indicative of increased risk of cardiovascular disease, and once again can be influenced by changes in diet and exercise. If you have the option, go for the high-sensitivity CRP (hsCRP) test if possible!

Know thy risk, and save thy life!

Everything that I have discussed in this post encompasses longevity technologies that are available to you NOW. And ultimately, it is up to YOU to demand access to these technologies, in one way or another. I’d suggest that you don’t take NO for an answer, and that you allocate whatever resources (time, energy, money) you have available to assessing and managing your risk of cardiovascular disease. If you are aged 50 or older, the importance of getting each of these tests performed is exponentially more important with each decade of life!

I hope you enjoyed this post. I’ll be sure to come along with my follow-up posts on the topic of the four deadly killers in the coming weeks. In the meantime, check-out these other great Lifeboat Foundation blog posts on the topic of aging, and don’t forget to checkout the Longevity Blog on my website.

Wishing you a long and healthy life!

Dr Nick Engerer

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In rich countries, more than 80% of the population today will survive past the age of 70. About 150 years ago, only 20% did. In all this while, though, only one person lived beyond the age of 120. This has led experts to believe that there may be a limit to how long humans can live.

Animals display an astounding variety of maximum lifespan ranging from mayflies and gastrotrichs, which live for 2 to 3 days, to giant tortoises and bowhead whales, which can live to 200 years. The record for the longest living animal belongs to the quahog clam, which can live for more than 400 years.

If we look beyond the animal kingdom, among plants the giant sequoia lives past 3000 years, and bristlecone pines reach 5000 years. The record for the longest living plant belongs to the Mediterranean tapeweed, which has been found in a flourishing colony estimated at 100,000 years old.

Some animals like the hydra and a species of jellyfish may have found ways to cheat death, but further research is needed to validate this.

The natural laws of physics may dictate that most things must die. But that does not mean we cannot use nature’s templates to extend healthy human lifespan beyond 120 years.

Putting a lid on the can

Gerontologist Leonard Hayflick at the University of California thinks that humans have a definite expiry date. In 1961, he showed that human skin cells grown under laboratory conditions tend to divide approximately 50 times before becoming senescent, which means no longer able to divide. This phenomenon that any cell can multiply only a limited number of times is called the Hayflick limit.

Since then, Hayflick and others have successfully documented the Hayflick limits of cells from animals with varied life spans, including the long-lived Galapagos turtle (200 years) and the relatively short-lived laboratory mouse (3 years). The cells of a Galapagos turtle divide approximately 110 times before senescing, whereas mice cells become senescent within 15 divisions.

The Hayflick limit gained more support when Elizabeth Blackburn and colleagues discovered the ticking clock of the cell in the form of telomeres. Telomeres are repetitive DNA sequence at the end of chromosomes which protects the chromosomes from degrading. With every cell division, it seemed these telomeres get shorter. The result of each shortening was that these cells were more likely to become senescent.

Other scientists used census data and complex modelling methods to come to the same conclusion: that maximum human lifespan may be around 120 years. But no one has yet determined whether we can change the human Hayflick limit to become more like long-lived organisms such as the bowhead whales or the giant tortoise.

What gives more hope is that no one has actually proved that the Hayflick limit actually limits the lifespan of an organism. Correlation is not causation. For instance, despite having a very small Hayflick limit, mouse cells typically divide indefinitely when grown in standard laboratory conditions. They behave as if they have no Hayflick limit at all when grown in the concentration of oxygen that they experience in the living animal (3–5% versus 20%). They make enough telomerase, an enzyme that replaces degraded telomeres with new ones. So it might be that currently the Hayflick “limit” is more a the Hayflick “clock”, giving readout of the age of the cell rather than driving the cell to death.

The trouble with limits

The Hayflick limit may represent an organism’s maximal lifespan, but what is it that actually kills us in the end? To test the Hayflick limit’s ability to predict our mortality we can take cell samples from young and old people and grow them in the lab. If the Hayflick limit is the culprit, a 60-year-old person’s cells should divide far fewer times than a 20-year-old’s cells.

But this experiment fails time after time. The 60-year-old’s skin cells still divide approximately 50 times – just as many as the young person’s cells. But what about the telomeres: aren’t they the inbuilt biological clock? Well, it’s complicated.

When cells are grown in a lab their telomeres do indeed shorten with every cell division and can be used to find the cell’s “expiry date”. Unfortunately, this does not seem to relate to actual health of the cells.

It is true that as we get older our telomeres shorten, but only for certain cells and only during certain time. Most importantly, trusty lab mice have telomeres that are five times longer than ours but their lives are 40 times shorter. That is why the relationship between telomere length and lifespan is unclear.

Apparently using the Hayflick limit and telomere length to judge maximum human lifespan is akin to understanding the demise of the Roman empire by studying the material properties of the Colosseum. Rome did not fall because the Colosseum degraded; quite the opposite in fact, the Colosseum degraded because the Roman Empire fell.

Within the human body, most cells do not simply senesce. They are repaired, cleaned or replaced by stem cells. Your skin degrades as you age because your body cannot carry out its normal functions of repair and regeneration.

To infinity and beyond

If we could maintain our body’s ability to repair and regenerate itself, could we substantially increase our lifespans? This question is, unfortunately, vastly under-researched for us to be able to answer confidently. Most institutes on ageing promote research that delays onset of the diseases of ageing and not research that targets human life extension.

Those that look at extension study how diets like calorie restriction affect human health or the health impacts of molecules like resveratrol derived from red wine. Other research tries to understand the mechanisms underlying the beneficial effects of certain diets and foods with hopes of synthesising drugs that do the same. The tacit understanding in the field of gerontology seems to be that, if we can keep a person healthy longer, we may be able to modestly improve lifespan.

Living long and having good health are not mutually exclusive. On the contrary, you cannot have a long life without good health. Currently most ageing research is concentrated on improving “health”, not lifespan. If we are going to live substantially longer, we need to engineer our way out of the current 120-year-barrier.

Avi Roy does not work for, consult to, own shares in or receive funding from any company or organisation that would benefit from this article, and has no relevant affiliations.

Read the original article.

I want to live longer and help others do the same. I assumed the most effective way to do that is by understanding the science of aging and then engineering solutions to extend human lifespan. That is why I became a biomedical researcher and over the past several years I have pursued this goal almost single-mindedly.

When a 2004 study showed that reducing the calorie intake in mice extended their life by 42%, I enthusiastically embraced the results and even put myself on a calorie restricted diet. But, subsequently, a 2012 study showed that long-term calorie restriction may not have the promised benefits. On the contrary, fewer calories without the required nutrients might actually cause harm.

Calorie restriction is not the first such “promising” route that eventually did not live up to the promise, and it will not be the last. Antioxidants showed promise in holding back diseases caused by aging, but now we know that antioxidant supplements are more likely to shorten your life.

Earlier in May, researchers showed that reducing a protein called NF-kB in mouse brains modestly improved their lifespan. I am not holding out for this result either. Before too long, I’m sure there will be reports of severe side effects of manipulating levels of NF-kB.

Take it easy

Looking at the data I have come to the conclusion that “doing nothing” may be the best option in most cases. This may not be as pessimistic as it sounds and it is definitely not to say that research in fighting aging must not be carried out.

When I say “do nothing”, I am assuming that you do not smoke or drink too much alcohol, and have access to medical care in case of injury. Such measures are bound to increase your lifespan.

But currently, not intervening in the aging process is more likely to help you live longer than trying any of the methods I’ve mentioned, not by a few months but by many years. Trying any of those interventions may actually cause harm, and will do so for the foreseeable future.

Lesson from the past

The chart below shows the survival rates – the percentage of the population that lives to a certain age – for men in England and Wales from 1860 to 2010.

In the 1860s, more than 20% of children died at birth or soon after. On average, men’s health started to decline around the age of 30, and only about 20% of the population survived for more than 70 years.

By 1910, child mortality decreased, thanks to improvements in hygiene and better medical care. This meant more men lived past the age of 50. Circle A shows this reduction in childhood mortality between 1860 and 2010. But, as can be seen from Circle D, the gain towards the end was not significant. This is because only 30% of males passed the age of 70.

Fifty years later, after the discovery of penicillin and invention of more vaccines, 90% of English and Welsh men lived until 50, and more than half survived to 70. Arrow B marks this trend.

Today almost 80% of men live to the age of 70. Four times as many men reach 70 now than in 1860.

What accounts for the change? Between 1860 and 1960, the significant increase in survival rate was due to medical intervention. Since 1960, the survival curve has improved mainly due to reduction in smoking.

This trend is similar in many rich countries, including the US. Druin Burch, a physician and writer, says in his book Taking the Medicine, that eliminating smoking would provide more benefits than being able to cure people of every possible type of cancer.

Age gracefully

Many experts believe that human lifespan might actually have an upper limit of 125 years. The average may not increase much beyond 90. If we are to agree with them, this leaves little room for improvement.

But we have never concentrated on maximising human lifespan before. Most people believe human lifespan is finite, so all drugs being manufactured today are targeted towards certain age-related diseases such as diabetes and hypertension. They are not designed to extend human lifespan.

If this bleak outlook is indeed true, we should not practise naive interventionism because it is unlikely to help. As Nassim Nicholas Taleb describes in his book Antifragile, naive interventionism occurs when we try to fix a single thing, but end up disturbing a complex system.

In case of extending human lifespan, those naive interventions would include calorie restriction, antioxidant supplements or manipulating the protein NF-kB, as mentioned earlier. They also include the current obsession with replacing fat in foods with sugar, the health benefits of drinking red wine, or the use ofsurgery or supplements to “fight” aging. This latter industry has grown in the past decade from being non-existent to an estimated worth of $88 billion today.

If intervening in the aging process with current biomedical science has any positive effect at all, it will be far too small to worry about. It’s far more likely to harm us.

That is why I have decided to do nothing and follow a simple rule: unless I meet with an accident, or suffer from a terminal disease, I will not add anything to my life with the explicit purpose of extending it. To do anything else would most likely do more harm than good.

Avi Roy does not work for, consult to, own shares in or receive funding from any company or organisation that would benefit from this article, and has no relevant affiliations.

This article was originally published at The Conversation.
Read the original article.

It is known, for example, that serious long-term CR dramatically lowers insulin levels.¹ Another hormone, with a similar molecular structure, insulin-like growth factor one (IGF-I), shares the same pathway with insulin and is downregulated by CR in animal studies and by calorie restricted humans who do not follow high protein diets.²

And there’s the rub. For if you hope to benefit from calorie restriction and do not pay attention to the special properties of macronutrient intake, individual foods, and food preparation, you may get an unpleasant surprise: excessive stimulation of the insulin/IGF-I pathway. For example, in a study using healthy volunteers, just 50 grams of white potato starch sends glucose and insulin soaring³ to levels associated with increased risk of cancer, heart disease and diabetes.⁴

Back in the 1930s, when the term calorie restriction was first applied to Dr. Clive McCay’s rat and mouse experiments,⁵ it was entirely appropriate because the focus was on calories since he was looking at growth retardation. Of course, little was known about the signals involved in the life-extending effects of the diet. All that changed as scientists discovered important cell-signaling patterns that produce the phenomenal life-transforming effects.⁶

In 2008, The CR Way took the latest CR science and crafted it into a holistic lifestyle that makes following a CR diet easier by transforming it into a happy, positive lifestyle that focuses on living better now and quite possibly living longer. Recipes, food choices, and lifestyle are deliciously and strategically planned to reduce the insulin / IGF-I pathway activity – making disease risk plummet, while increasing the probability of a longer life.
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1. Fontana L, Meyer T.E., Klein S, Holloszy J.O. Long-Term Calorie Restriction Is Highly Effective In Reducing The Risk For Atherosclerosis In Humans. Proceedings of the National Academy of Science USA 2004;101(17):6659–6663.
2. Fontana L, Klein S, Holloszy J.O. Long-term low-protein low-calorie diet and endurance exercise modulate metabolic factors associated with cancer risk. American Journal of Clinical Nutrition. 2006;84:1456–62.
3.Brand-Miller JC, et al. Mean changes in plasma glucose and insulin responses in 10 young adults after consumption of 50g carbohydrates from potato (high-glycemic index; GI) or barley (low-GI) meal. American Journal of Clinical Nutrition. 2005 Aug;82(2):350–4
4. Guideline for Management of Post-meal Glucose, International Diabetes Federation, 2007 ISBN 2–930229-48–9
5. McCay CM, Crowell MF, Maynard LA. Journal of Nutrition. l0:63–79, 1935
6. McGlothin PS, Averill MS. Advances in Calorie restriction. Antiaging Medicine. 2009 Aug;4(4):440–441