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What Is Garam Masala and How Can You Use It?

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Sometimes dubbed “the magic spice,” garam masala is actually a blend of spices mixed into one.1 There is no one way to prepare this spice; it varies from region to region, and from one household to another.2 This article will delve deeper into garam masala, including what it’s made of, how to use it properly and what dishes you can add it to.

What Is Garam Masala?

To some, Indian cuisine is an adventure — the dishes from this country have a vibrant and unique quality about them, owing to their bright colors and intense flavors. This is mainly due to their love of spices, and one prominent staple is garam masala.

“Garam masala” hails from two Indian words: “garam,” which means “hot,” and “masala,” which translates to “spice mixture.”3 It’s believed to have originated from northern India, which is prone to cold temperatures,4 and is often added to dishes like curries and soups or to enhance the flavor of foods like lentils.5

Surprisingly, garam masala isn’t completely spicy.6 Its flavor is warm and aromatic rather than fiery hot like curry.7 In an editorial published in The Economic Times, the author notes that the “hot” component of this spice blend may refer to fact that the spices composing it are all considered “heating” to the body, meaning they all have the ability to improve your metabolism.8

As mentioned above, this blend can be made in various ways. The Spruce Eats notes that some traditional garam masala ingredients include:9

  • Black pepper
  • Cardamom
  • Nutmeg

Other variations make use of spices like garlic, ginger, fennel seeds, bay leaves, fenugreek, tamarind, mustard seeds, star anise, mace and Malabar leaves.10 Garam masala is either used on its own or added to dishes along with other spices. This mixture is often preroasted before being used — this unlocks and deepens the flavors and aroma of the spices.11

Garam masala is often compared to curry powder. The word “curry” is believed to be an 18th century British invention, and that the curry most Westerners know today is referred to simply as “masala” in India — their day-to-day spice blend.12 There are plenty of theories on the origin of this word, one of which is that the British took it from the Tamil word “kari,” which refers to a dish paired with rice.13

4 Spices in Garam Masala and Their Health Benefits

I’ve mentioned before that flavoring your food with herbs and spices is a simple way of upgrading the nutrient density of your meals without adding any calories. You’ll be pleased to know that many of the spices used in garam masala offer their own set of health benefits. Here are some examples:

1. Black pepper — Known for its anti-inflammatory and gastroprotective properties, black pepper contains an active compound called piperine.14 For people aiming to reduce their waist size and body fat, as well as to maintain optimal cholesterol levels, piperine may be beneficial due to its ability to inhibit the formation of new fat cells.15

2. Cinnamon — This spice, loved for its delicious flavor and fragrance, has been found to be beneficial for diabetics because it may help reduce blood glucose levels and improve insulin resistance. A 2003 study published in Diabetes Care journal stated that:16

“[I]ntake of 1, 3, or 6 g of cinnamon per day reduces serum glucose, triglyceride, LDL cholesterol, and total cholesterol in people with Type 2 diabetes … [T]he inclusion of cinnamon in the diet of people with Type 2 diabetes will reduce risk factors associated with diabetes and cardiovascular diseases.”

3. Cloves — A 2008 study published in the Journal of Medicinal Foods revealed that there’s a direct correlation between the antioxidant content of certain extracts from spices and herbs and their ability to block advanced glycation end (AGE) products, which in turn helps minimize the risk of heart disease and inhibit premature aging. Of all the 24 herbs and spices tested, cloves ranked the most potent in producing these effects.17

4. Cardamom — Studies show that cardamom, which is related to cinnamon, may help optimize your insulin and cholesterol levels, and help lower blood glucose levels.18 It also boasts of antimicrobial and anti-inflammatory properties, which help promote better metabolic function and soothe your gastrointestinal system.19

Garam Masala Uses

In India, the way garam masala is used depends on the region. The Spruce Eats notes that in northern India, it’s used in powder form, while in southern areas, it’s mixed with water, vinegar or coconut milk to form a paste. Garam masala blends from southern regions also tend to be spicier than those from northern areas, mainly because of the hotter climate and increased exposure to sunlight, leading to higher levels of capsaicin to develop in chiles.20

According to the Kitchn, garam masala’s warm flavor blends well with various meat, poultry and vegetable dishes. It also works great in soups, curries and lentils. One tip when using garam masala is to add it at the end of the cooking, when the heat is already turned off.21 Less exposure to heat helps preserve the flavor of the spices.

How to Make Garam Masala Spice: Recipes You Can Make at Home

Spices used for traditional garam masala are ground fresh daily to ensure that their rich flavors and aromas stay intact.22 You can use either fresh whole spices or preground spices, but remember that using preground spices will not be as flavorful, since their quality has already deteriorated.

Remember, there’s no single way to make this spice blend, as each recipe and household makes use of different spices and in varying ratios. Here are a couple of homemade garam masala recipes you can follow:

Garam Masala Recipe

Yield: 1 1/2 cups Prep Time: 5 minutes Cook Time: 5 minutes Total Time: 10 minutes

Ingredients

  • 3 tablespoons cumin seeds
  • 2 tablespoons coriander seeds
  • 1 1/2 tablespoons fennel seeds
  • 1 tablespoon black cumin seeds
  • 1/4 cup black cardamom
  • 2 tablespoons green cardamoms
  • 2 tablespoons black peppercorns
  • 1 tablespoon cloves
  • 5-inch cinnamon stick
  • 1 1/2 tablespoons mace
  • 15 pieces bay leaves
  • Half a nutmeg
  • 2 1/2 teaspoons dry ginger powder

Procedure

  1. Dry roast the spices (except for the ginger powder) over low-medium heat for two to three minutes. You do not want any color change — you only need to warm up the spices to eliminate any moisture.
  2. Another way is to spread the spices outdoors and leave them under the sun for a day.
  3. Allow the spices to cool down completely. Once cool, place the spices in a spice grinder or coffee grinder along with the ginger powder and grind. You can do this in batches if you have a small grinder.
  4. The grinding can make the spices warm, so once they’re finished, place them on a plate and let them cool before storing in an airtight container. This can stay good for eight months to a year.

(Recipe from Spice Up the Curry23)

Garam Masala Powder

Serving Size: About 1/3 cup

Ingredients

  • 6 to 8 green cardamom pods, green husks removed and discarded
  • 2 tablespoons whole coriander seed
  • 1 tablespoon whole cumin seed
  • 1 tablespoon whole black peppercorns
  • 1 teaspoon whole cloves
  • 1 teaspoon fennel seeds
  • 1 3-inch stick of cinnamon
  • 1 star anise pod
  • 1/2 teaspoon ground nutmeg or mace

Procedure

  1. Put the cardamom, cumin, coriander, cloves, peppercorns, cinnamon, fennel and anise in a medium skillet over medium heat. Cook, tossing frequently, until aromatic and toasted-smelling, about two minutes.
  2. Transfer to a spice grinder or mortar and pestle, and then add ground nutmeg. Grind into a fine powder.

(Recipe from Serious Eats24)

Garam Masala Spice Recipes You Can Try

Once your garam masala spice mix is ready, you can now start cooking. Here are a couple of recipes you can make at home.

Chicken Tikka Masala With Cauliflower Rice

Prep Time: 10 minutes Cook Time: 15 minutes Servings: 2

Ingredients

  • 1 free-range chicken breast (skin on, about 3 ounces)
  • 1/2 tablespoon garam masala
  • 1 tablespoon coconut oil
  • 4 tablespoons coconut cream
  • 2 tablespoons heavy cream
  • 1 teaspoon ginger grated
  • 1 teaspoon garlic powder
  • 1 clove garlic minced
  • 1 tablespoon tomato paste
  • 1 teaspoon paprika
  • Fresh cilantro, to garnish
  • 1 teaspoon salt

Procedure

  1. Dice the chicken breasts into bite-sized chunks. Over medium heat, pan fry in heated coconut oil for approximately five minutes.
  2. Combine the heavy cream and coconut cream in the pan and let simmer another two minutes.
  3. Add the garlic cloves, garlic powder, ginger, garam masala and tomato paste, and then stir the chicken in.
  4. Season with paprika and salt, and mix properly to fully combine. Let simmer for five more minutes. Take away from heat.
  5. Serve over the cauliflower rice and some chopped cilantro on top. Enjoy.

(Recipe adapted from KetoVale.com25)

Low-Carb Lamb Masala With Okra

Prep Time: 5 minutes Cook Time: 1 hour Servings: 2

Ingredients

  • 1 tablespoon coconut oil
  • 1 tablespoon garam masala
  • 1/4 cup chopped onion
  • 2 lamb shoulders, bones removed, trimmed and chopped
  • 8 ounces tomato sauce
  • 1 teaspoon garlic paste
  • 1 teaspoon ginger paste
  • 8 fluid ounces of water
  • 1/2 cup chopped okra
  • 2 tablespoons plain Greek yogurt
  • Salt to taste
  • Fresh chopped cilantro to garnish

Procedure

  1. In a large pan, heat the coconut oil and add the garam masala, and cook for two to three minutes until fragrant.
  2. Add lamb and onion, and allow to cook until the onion has softened and the meat has browned, around two to three minutes.
  3. Add tomato sauce, garlic, water and ginger, and bring to a boil, then reduce to a simmer.
  4. Cover and cook for 35 to 40 minutes until the sauce has reduced and thickened.
  5. Add yogurt and okra. Allow to cook four to five minutes, until the okra is tender.
  6. Check the seasoning and add more salt if needed. Garnish with chopped cilantro and serve.

(Recipe adapted from Sleep Away from the Carbs26)

How to Store Garam Masala

Remember that the aromatic qualities of spices come from the essential oils they contain. Unfortunately, these oils lose their flavor easily and are highly volatile.27 NDTV Food lists some other helpful tips for storing garam masala and other spices to prolong their shelf life:28

1. Place the spice in an airtight jar — Moisture in the air can lead to the garam masala losing its aroma, flavor and color.

2. Do not store it near heat or under bright light — You may be tempted to have your garam masala and other spices beside the stove so they’re within arm’s length while you’re cooking, but this will cause them to lose their flavor. It’s best to keep them away from heat and light sources such as sunlight. Instead, put them in a closed cupboard. A cool and damp area is the best place for herbs and spices.

3. Do not place it in the refrigerator — Garam masala may be fine in the fridge for a day or two, but once it builds up moisture, it will lose its aroma.

4. Keep it away from water — Even a few drops can affect the flavor and aroma of your masala. Always use a clean, dry spoon whenever scooping out the spice.

Garam Masala Substitutes

Garam masala isn’t a mix that you can make with just a few ingredients — you’ll need to have several whole spices on hand to make sure you get an authentic blend that will complement your meals. However, if you’re in a pinch and cannot make it, Gourmet Sleuth recommends combining one part cumin powder with one-fourth part allspice powder, which will mimic the flavor of this spice blend.29

I still recommend making your own garam masala from scratch, using whole spices instead of buying bottled powdered spices. Not only are you able to tweak the flavor according to your preferences, but you can also be certain that you’re only using wholesome ingredients. It may require some time and effort, but the resulting flavor and aroma from your dishes will be worth it!

Garam Masala Frequently Asked Questions

Q: What is in garam masala?

A: Garam masala contains a number of spices. The variations are endless, and vary from region to region, and from one household to another. Some common spices used for traditional garam masala include black pepper, cinnamon, coriander, cloves, nutmeg, cumin and cardamom. Other spices that can be used include star anise, fennel seeds, ginger and garlic.

Q: Where can I buy garam masala?

A: There are garam masala powders sold in grocery stores and online shops today, but if you prefer a healthier and more authentic version, I recommend buying whole spices and making your own blend at home.

Q: Is garam masala spicy?

A: Garam masala is not necessarily spicy, but rather warm and aromatic. Although “garam” translates to “hot,” this term may actually be referring to the “warming” or metabolism-boosting properties of the spices, and not the flavor.

Q: Can you make your own garam masala?

A: Yes, you can. There are numerous recipes you can try. Feel free to experiment with the ratios and the spices variations so you can find a blend that suits your taste.

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LEAF Interviews David Sinclair

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David Sinclair recently published a new book to assist in publicizing his present research directions, companies, and thinking on aging, and is here interviewed by the Life Extension Advocacy Foundation (LEAF) volunteers. The work presently underway includes supplements to increase levels of NAD+ in mitochondria and, separately, partial reprogramming of cells in a living individual in order to gain some of the effects of full reprogramming, particularly restoration of mitochondrial function. Fully reprogramming cells into induced pluripotent stem cells has been shown to clear out dysfunctional mitochondria and reset epigenetic markers of age to a more youthful configuration.

It is worth noting that this strategy will not be able to fix a great many of the issues that arise in cells with age, such as the accumulation of metabolic waste that even youthful cells cannot break down effectively. If it can be used to safely restore mitochondrial function in old tissues for an extended period of time, however, then that is certainly interesting enough to chase aggressively in and of itself. Mitochondrial dysfunction is a noteworthy aspect of aging, and is involved in numerous age-related diseases.


Currently, medicine treats the symptoms, not the causes, of age-related diseases. Do you think that we might soon reach the point where therapies will be taken in a preventive manner to delay the onset of age-related diseases?

Well, there’s a subset of the population, particularly in the US, but increasingly around the world, who are using the internet to educate themselves and are trying to take action before they become sick. Sometimes with medical supervision, sometimes not. It’s a grassroots movement right now; for it to become mainstream, the regulations would have to change so that doctors can feel comfortable prescribing medicines to prevent diseases. But, if we don’t change, then we will continue to practice whack-a-mole medicine and only treat one disease at a time after it’s already developed.

You are very well known for your work with NAD+ and its precursors; we’re often asked whether nicotinamide riboside or nicotinamide mononucleotide is better?

They’re very similar molecules, and both have been shown to provide a variety of health benefits in mice. That doesn’t mean either of them will work to slow aging in humans, and that’s why placebo-controlled clinical trials are required to know if one of them, or both of them, will work in certain conditions. Those studies began over a year ago, and they are currently Phase 1 safety studies in healthy volunteers. Next year, the plan is to test the pharmaceutical product in a disease area, most likely a rare disease, but also in the elderly to see if we can recapitulate some of the results we’ve seen in mice, such as increased blood flow and endurance.

Another area that you are involved in is partial cellular reprogramming to reverse age-related epigenetic alterations in cells and tissues. Please tell us a little bit about this approach and the approach that you are taking and how you’re progressing so far?

For 20 years, we’ve been working on epigenetic changes as a cause of aging, starting with work in yeast and now in mammals. We’ve developed viral vectors and combinations of reprogramming factors that appear to be much safer than past approaches, and we’ve used them to reprogram the eye to restore vision in mice with glaucoma and in very old mice. Currently, it is believed that the epigenetic clock is just an indicator of age and not part of the actual aging process, but our recent work strongly suggests that the process of reversing the clock doesn’t just change the apparent age of the body, it actually reverses aging itself by restoring the function of the old cells to behave as though they’re young again. Therefore, the clock may not just be telling time; it may actually be controlling time.

Could you please tell us a little bit about your book and what the readers should look forward to?

Lifespan: Why We Age and Why We Don’t Have To” takes the reader on a journey through history, looking at the endeavor of humans to try to live longer and using that historical perspective to look at today’s situation and project into the future. The book also takes readers on a journey through the very cutting edge of aging research and things that the reader can do right now to take advantage of these new discoveries in their daily lives with changes in their daily activity, what they eat, when they eat, but also medicines that are currently available on the market that may extend lifespan. The last chapter is about where we are headed, what are the medicines that are in development, and then when these drugs become available, what does the world look like? Is it a better place or a worse place, and how will our lives change?

Link: https://www.leafscience.org/an-interview-with-dr-david-sinclair/

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Repair of a Damaged Cornea Using Cells Derived from Induced Pluripotent Stem Cells

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Since the discovery of induced pluripotency more than a decade ago, researchers have been working towards the use of this technology to produce cells for use in tissue engineering and regenerative therapies. Induced pluripotent stem cells are functionally equivalent to embryonic stem cells; given suitable recipes and methods for the surrounding environment and signals, they can be made to generate any of the cell types in the body. The cornea of the eye is a comparatively simple starting point for tissue engineering, easier to work with in many ways, in generating tissues and in delivering cells to the patient. Here, the first repair of a human cornea is reported, using tissue structures produced from induced pluripotent stem cells.


A Japanese woman in her forties has become the first person in the world to have her cornea repaired using reprogrammed stem cells. The woman has a disease in which the stem cells that repair the cornea, a transparent layer that covers and protects the eye, are lost. The condition makes vision blurry and can lead to blindness. To treat the woman, researchers created sheets of corneal cells from induced pluripotent stem (iPS) cells. These are made by reprogramming adult skin cells from a donor into an embryonic-like state from which they can transform into other cell types, such as corneal cells.

The woman’s cornea remained clear and her vision had improved since the transplant a month ago. Currently people with damaged or diseased corneas are generally treated using tissue from donors who have died, but there is a long waiting list for such tissue in Japan. Japan has been ahead of the curve in approving the clinical use of iPS cells, which were discovered by stem-cell biologist Shinya Yamanaka. Japanese physicians have also used iPS cells to treat spinal cord injury, Parkinson’s disease, and another eye disease. The Japanese health ministry gave permission to try the procedure on four people. The team is planning the next operation for later this year and hope to have the procedure in the clinic in five years.

Link: https://doi.org/10.1038/d41586-019-02597-2

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Short Term versus Long Term Gains in Working Memory Following Exercise

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Research has established that exercise rapidly produces an improvement in memory function, within a matter of minutes. It is also the case that regular exercise slows cognitive decline with age and taking up exercise improves cognitive function in older individuals, when considered over the long term rather than immediately following exercise. Given that only a minority of the population in wealthier parts of the world, and particularly the older segment of the population, exercise to the degree recommended to best maintain health, these findings should probably be considered more a case of people doing themselves harm than a case of there being benefits to be obtained.

Today’s research materials are interesting for directly comparing the short term and long term benefits of exercise to the operation of working memory in older people. The effect size is about the same, in that the same degree of improvement is observed immediately following exercise versus after a period of regular exercise, but the former benefit is very short-lived, while the latter benefit is sustained over time. The short-term benefit is also only observed in some people, and those differences correlated with structural differences in the brain. Is this all of any practical use at the present time, beyond being yet another recommendation to undertake more exercise? Probably not, but in the long term there is no such thing as useless knowledge.

New study suggests exercise is good for the aging brain


Researchers have found that a single bout of exercise improves cognitive functions and working memory in some older people. In experiments that included physical activity, brain scans, and working memory tests, the researchers also found that participants experienced the same cognitive benefits and improved memory, for a short time, from a single exercise session as they did in a sustained fashion from longer, regular exercise.

Previous research has shown exercise can confer a mental boost. But the benefits vary: One person may improve cognitively and have improved memory, while another person may show little to no gain. Limited research has been done on how a single bout of physical activity may affect cognition and working memory specifically in older populations, despite evidence that some brain functions slip as people age. Researchers wanted to tease out how a single session of exercise may affect older individuals. The team enrolled 34 adults between 60 and 80 years of age who were healthy but not regularly active. Each participant rode a stationary bike on two separate occasions – with light and then more strenuous resistance when pedaling – for 20 minutes. Before and after each exercise session, each participant underwent a brain scan and completed a memory test.

After a single exercise session, the researchers found in some individuals increased connectivity between the medial temporal lobe (which surrounds the brain’s memory center, the hippocampus) and the parietal cortex and prefrontal cortex, two regions involved in cognition and memory. Those same individuals also performed better on the memory tests. Other individuals showed little to no gain. The boost in cognition and memory from a single exercise session lasted only a short while for those who showed gains, the researchers found.

The participants also engaged in regular exercise, pedaling on a stationary bike for 50 minutes three times a week for three months. One group engaged in moderate-intensity pedaling, while another group had a mostly lighter workout in which the bike pedals moved for them. Most individuals in the moderate and lighter-intensity groups showed mental benefits, judging by the brain scans and working memory tests given at the beginning and at the end of the three-month exercise period. But the brain gains were no greater than the improvements from when they had exercised a single time.

Acute Exercise Effects Predict Training Change in Cognition and Connectivity


Previous studies report memory and functional connectivity of memory systems improve acutely after a single aerobic exercise session or with training, suggesting the acute effects of aerobic exercise may reflect initial changes that adapt over time. In this trial, for the first time, we test the proof-of-concept of whether the acute and training effects of aerobic exercise on working memory and brain network connectivity are related in the same participants. Cognitively normal older participants (N=34) were enrolled in a randomized clinical trial. Participants completed fMRI resting state and a working memory task acutely after light and moderate intensity exercise and after a 12-week aerobic training intervention.

Functional connectivity did not change more after moderate compared with light intensity training. However, both training groups showed similar changes in cardiorespiratory fitness (maximal exercise oxygen uptake, VO2peak), limiting group-level comparisons. Acute effects of moderate intensity aerobic exercise on hippocampal-cortical connections in the default network predicted training enhancements in the same connections. Working memory also improved acutely, especially following moderate intensity, and greater acute improvements predicted greater working memory improvement with training. Exercise effects on functional connectivity of right lateralized fronto-parietal connections were related to both acute and training gains in working memory.

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Statins Shown to Extend Life by Mere Days

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Researchers have repeatedly failed to find evidence that high cholesterol is a risk factor for cardiovascular disease. In fact, there’s plenty of evidence suggesting that higher cholesterol may actually be healthier than lower levels.

As I’ve discussed in many previous articles, three (to some degree interrelated) factors that have a far greater influence on your cardiovascular disease (CVD) risk are:

Elevated iron levels will significantly contribute to inflammation, but even if your iron is normal, chronic inflammation can be caused by a wide range of factors, starting with your diet. Your diet is also the key factor at play when it comes to your insulin level, and can worsen the effects of iron overload.

Unfortunately, these primary contributors are rarely the focus of CVD prevention and treatment in conventional medicine. Instead, statins (cholesterol lowering drugs) are the go-to first line of defense, and this despite the many studies showing cholesterol isn’t a part of the problem.

Eye-Opening Finding: Statins Extend Life by About Three Days

A systematic review4 published in 2015 that deserves far more attention than it has received assessed the ability of statins to postpone death and improve mortality rates. Eleven statin trials with a follow-up between two and 6.1 years were included in the review.

In primary prevention trials (meaning studies in which statins were used as a primary prevention for CVD), death was postponed between a negative five days (meaning they died five days sooner than the control group) and 19 days.

In secondary prevention trials, death was postponed between a negative 10 days and 27 days. The median postponement of death in primary prevention trials was 3.2 days, and in secondary prevention trials 4.1 days.

This is a truly astounding finding, considering people take stains for years, if not decades, and the fact that these drugs are associated with a wide range of serious side effects that can decimate quality of life.

British MP Calls for Parliamentary Inquiry Into Statins

The good news is, more and more scientists are now starting to see this truth. A March 9, 2019, article5 in European Scientist reported:

“Earlier this week, the Chair of the British Parliament Science and Technology Committee, Sir Norman Lamb MP made calls for a full investigation into cholesterol lowering statin drugs.

It was instigated after a letter was written to him signed by a number of eminent international doctors including the editor of the BMJ, the Past President of the Royal College of Physicians and the Director of the Centre of Evidence Based Medicine in Brazil … calling for a full parliamentary inquiry into the controversial medication.”

In the article, the lead author of the letter, cardiologist Aseem Malhotra, discusses the dangers of statins, and how the flawed cholesterol hypothesis and the corresponding low-fat myth are pushing patients’ health in the wrong direction. He writes, in part:6

“It is not just financial interests that bias research findings but also intellectual hubris in medicine too. It was the father of the evidence based medicine movement the late Professor David Sackett who said ‘Fifty percent of what you learn in medical school will turn out to be either outdated or dead wrong within five years of your graduation, the trouble is no one can tell you which half so you have to learn to learn on your own.’

In the past 30 years, there have now been 44 randomized controlled trials that reveal no cardiovascular mortality benefit from diet or various drug trials from lowering cholesterol.

Most conspicuous was the recent ACCELERATE trial with over 12,000 patients at high risk of heart disease that revealed no reductions in heart attack, stroke or death despite a 37% reduction in LDL-cholesterol.

But how many doctors actually keep up with the latest evidence? Many will defend the cholesterol lowering dogma with their more inquisitive patients by saying they’re just following guidelines, unaware that the guidelines themselves are based upon biased research often written by scientists with strong personal or institutional financial ties to the industry.”

Scientific Review Declares Statin Claims Are Overblown

Another newsworthy review7 that ties into Malhotra’s arguments against statins was published in the Expert Review of Clinical Pharmacology in September 2018. It identified significant flaws in three recent studies “published by statin advocates” attempting “to validate the current dogma.”

The paper presents substantial evidence that total cholesterol and low-density lipoprotein (LDL) cholesterol levels are not an indication of heart disease risk, and that statin treatment is of “doubtful benefit” as a form of primary prevention for this reason. The paper also details the tactics used in statin studies to exaggerate the benefits. Among them:

Excluding unsuccessful trials where statins either had no or negative impact on CVD risk or mortality

Using “evidence” that isn’t a true exposure-response

Cherry-picking data that supports the conclusion of benefit

Ignoring the most important outcome — an increase in life expectancy

Using a statistical tool called relative risk reduction to amplify trivial effects — This was also addressed more directly in a 2015 report8,9 titled “How Statistical Deception Created the Appearance That Statins Are Safe and Effective in Primary and Secondary Prevention of Cardiovascular Disease.”

Here, the authors point out that if you look at absolute risk, statin drugs benefit just “1% of the treated participants.”10 This means that out of 100 people treated with the drugs for five years, one person will have one less heart attack.

According to the authors of the 2018 review:11

“For some years, many researchers have questioned the results from statin trials because they have been denied access to the primary data. In 2004–2005, health authorities in Europe and the United States introduced New Clinical Trial Regulations, which specified that all trial data had to be made public. Since 2005, claims of benefit from statin trials have virtually disappeared.”

How Statin Studies Minimize Appearance of Side Effects

The Expert Review of Clinical Pharmacology paper also points out that statin trials minimize health risks by using a run-in period. Essentially, the participants are given the drug for a few weeks, after which those who suffer adverse effects are simply excluded.12 Needless to say, this automatically lowers the number of perceived side effects.

In reality, serious side effects may affect anywhere from 20% to 50% of statin users.13 What’s more, muscle damage is likely far more common a side effect than most statin studies claim.

The authors cite one study in which myopathy occurred in just 0.01% of treated individuals. However, myopathy was defined as having a creatine kinase level “more than 10 times higher than normal,” the authors note.14

Meanwhile, other research that looked at muscle biopsies found patients with normal creatine kinase levels, who complained of muscular symptoms, indeed had microscopic signs of myopathy. “When patients stopped treatment, their symptoms disappeared, and repeated biopsies showed resolution of the pathological changes,” the authors note, adding that:15

“To reject the frequent occurrence of muscular problems with the argument that muscle symptoms are nocebo effects is also invalid. In a study of 22 statin-treated professional athletes, the authors reported that 17 (77%) of the athletes terminated treatment because of muscular symptoms, which disappeared a few days or weeks after drug withdrawal.

The explanation for statin-induced adverse muscle effects is probably that statin treatment not only blocks the production of cholesterol but also blocks the production of several other important molecules, for instance, coenzyme Q10, which is indispensable for energy production.

As most energy is produced in the muscle cells, including those of the heart, the extensive use of statin treatment may explain the epidemics of heart failure that have been observed in many countries.”

Another study16 published in 2011 supports these statements, concluding that statin treatment lasting longer than two years causes “definite damage to peripheral nerves.”

A study17 published in the August 2019 issue of JACC: Basic to Translational Science presents a new mechanism of statin-induced myopathy. In short, the data suggest statin treatment causes calcium to leak out of your muscle cells.

As explained by Science Daily,18 “Under normal conditions, coordinated releases of calcium from these stores make the muscles contract. Unregulated calcium leaks may cause damage to muscle cells, potentially leading to muscle pain and weakness.”

Statin Use Is Associated With a Wide Variety of Problems

In their Expert Review of Clinical Pharmacology paper, the authors also highlight research showing statin use is associated with a number of significant health complications beside muscle problems:19

“… [C]ase–control and cross-sectional studies have shown that statin use is observed significantly more often among patients with cataracts, hearing loss, suicidal ideation, peripheral neuropathy, depression, Parkinson’s disease, interstitial cystitis, herpes zoster, impotency, cognitive impairments, and diabetes.

In some of these studies, the side effects disappeared with discontinuation of the statins and worsened with rechallenge. As cholesterol is a vital substance for the renewal of all cells, and since statins also block the production of other molecules necessary for normal cell function, it is not surprising that statin treatment may result in side effects from many different organs.”

Even More Reasons to Avoid Statin Drugs

The scientific fact is, aside from being a “waste of time” and not doing anything to reduce mortality, statins also come with a long list of potential side effects and clinical challenges. Importantly, statins:

1. Deplete your body of CoQ10 — Statins block HMG coenzyme A reductase in your liver, which is how they reduce cholesterol. But this is also the same enzyme that makes CoQ10, which is an essential mitochondrial nutrient that facilitates ATP production.

2. Inhibit the synthesis of vitamin K2, a vitamin that protects your arteries from calcification.

3. Because of 2 and 3, statins increase your risk for other serious diseases. Aside from the conditions mentioned above, they may also raise your risk for:

a. Cancer — Research20 has shown that long-term statin use (10 years or longer) more than doubles women’s risk of two major types of breast cancer: invasive ductal carcinoma and invasive lobular carcinoma.

b. Diabetes — Statins have been shown to increase your risk of diabetes via a number of different mechanisms, two of which include increasing your insulin resistance, and raising your blood sugar. According to one recent study,21statins double your risk of Type 2 diabetes, and triple the risk when taken for more than two years.

c. Cognitive dysfunction, neurological damage22 and neurodegenerative diseases, including vascular dementia, Alzheimer’s disease and Parkinson’s disease.23

d. Decreased heart function.24

e. Impaired fertility — Importantly, statins are a Category X medication,25 meaning they cause serious birth defects,26 so they should never be used by a pregnant woman or women planning a pregnancy.

Statins Do Not Benefit Patients With Respiratory Disease

Aside from lowering cholesterol, statins appear to have an ameliorating effect on inflammation. For this reason, statins are at times used in the treatment of pulmonary conditions such as chronic obstructive pulmonary disease (COPD). This may be because statins are a Nrf2 activator27 and decrease oxidative stress and secondary inflammation.

However, while some observational studies have shown a potential benefit, a July 2019 systematic review28 by the Cochrane Database of Systematic Reviews failed to find any significant benefit for this patient group. The review had three primary objectives:

a. To determine whether statins reduce mortality rates in COPD

b. To determine whether statins reduce exacerbation frequency, improve quality of life, or improve lung function in COPD

c. To determine whether statins are associated with adverse effects

The review included eight placebo-controlled studies involving 1,323 participants with COPD, with a mean age of 61.4 to 72 years. According to the authors:29

“We found no statistically significant difference between statins and placebo in our primary outcome of number of exacerbations per person‐year, including number of exacerbations requiring hospitalization per person‐year …

Our primary outcomes of all‐cause mortality and COPD‐specific mortality showed no significant difference between statins and placebo, with wide confidence intervals suggesting uncertainty about the precision of the results … Results show no clear difference in quality of life, which was reported in three trials …

A small number of trials providing low‐ or moderate‐quality evidence were suitable for inclusion in this review. They showed that use of statins resulted in a reduction in CRP and IL‐6, but that this did not translate into clear clinical benefit for people with COPD.” 

Beware: Next-Gen Cholesterol Drugs Likely Just as Harmful

While some of the dangers of statins are becoming more widely recognized, the dangers of cholesterol-lowering drugs in general is still being swept under the rug as newer drugs are being released.

One next-gen class of cholesterol-lowering drugs is the proprotein convertase substilisin/kexin type 9 (PSCK9) category, also known as PCSK9 Inhibitors.30 Just as there are many different drugs within the statin category, there are many in the PSCK9 category. Repatha is one of them.

PCSK9 is a protein that works with LDL receptors that regulate LDL in your liver and release LDL cholesterol into your blood. The inhibitors work by blocking that protein, thus lowering the LDL in circulation.

While these drugs are being touted as the answer for those who cannot tolerate some of the side effects of statins, such as severe muscle pain, there’s already evidence suggesting PCSK9 inhibitors can produce neurocognitive effects, with some patients experiencing confusion and attention deficits.31,32,33,34

At the end of the day, if you’re concerned about your heart health, you’d be wise to implement lifestyle changes known to support a healthy heart and help prevent CVD from developing in the first place. You can learn more about your risk factors, recommended tests and drug-free prevention methods in the following articles: “Cholesterol Does Not Cause Heart Disease,” “How to Increase Your Health Span,” and “Why Your Doctor Is Wrong About Cholesterol.”

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Why You See 9 Pharmaceutical Ads a Day

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The U.S. and New Zealand are the only two countries that allow pharmaceutical companies to advertise on TV or radio.1 Although the FDA had always allowed advertising, they also required that a long list of side effects be published at the same time. This was possible in newspaper advertising with small print, but in a 30-second TV ad it couldn’t be done.

It was during a speech at the American Advertising Federation conference when then FDA commissioner Arthur Hayes talked about drug advertising and said it2 “may be on the brink of exponential growth phase of direct-to-consumer promotion of prescription products.” This simple sentence was taken to mean the FDA may support direct-to-consumer (DTC) ads for pharmaceutical products.

In 1996, a TV spot from Schering-Plough for Claritin allergy medication promised “clear days and nights” and recommended the viewer “see your doctor” without mentioning what the product treated.3 The ad forced the FDA’s hand and they relaxed earlier guidelines, changing the requirements from an exhaustive list of side effects to a brief summary of the most important risks.

According to the FDA,4 advertising must also list at least one approved use and the generic name. Once this happened, it appeared there was no turning back. In 1998, one year after the decision, David Kessler, a past FDA commissioner, was speaking to a group of executives from Big Pharma, and warned:5

“Your companies likely will face lawsuits eventually about the claims they make for their products in television commercials. One day in a courtroom, I assure you, one of you is going to have your DTC ads played.”

There is no doubt these advertising campaigns are controversial and there are groups on both sides who adamantly defend their position. One underlying debate is the role consumers play in medical decisions6 and the time it may take from already limited time with a doctor.7 But, despite the arguments, it’s difficult to ignore the manipulation and financial gain associated with these campaigns.

US Is One of Two Countries Allowing Direct Ads

DTC advertising is big bucks — for Big Pharma and the media. While New Zealand currently allows the ads, large medical groups have come out with statements against them, calling for a total ban in much the same way the American Medical Association has.8

As consumers and advocates in the U.S. are battling Big Pharma and the media, New Zealand has taken aim at changing legislation.9 One agency claims 57% of consumers in New Zealand want the ads to stop10 but the country continues to allow the DTC selling of pharmaceuticals.

Dr. Michael Carome is director at Public Citizen,11 a nonprofit consumer advocacy organization boasting 500,000 members and supporters throughout the U.S.12 In an interview with Sharyl Attkisson on Full Measure,13 Carome discussed the billions of dollars pharmaceutical companies are spending each year on TV and radio ads, and the attendant repercussions on public health.

He claims most people who watch television every day will see up to nine pharmaceutical ads per day and up to 30 hours of pharmaceutical ads every year.14 Carome spoke about the role this plays in the fourth leading cause of death and injury in the U.S. — people taking prescription drugs as prescribed.

Thomas J. Moore, scientist at the Institute for Safe Medication Practices, notes there is no system for adding up the number of prescription drug deaths unrelated to a prescription error or overdose.15 Although it’s recommended that health care providers report complications to the FDA, the system is not mandatory.

According to Donald Light, a medical sociologist and author, about 2,460 people die each week as a result of taking prescription medications. To clarify, this is separate from those who died from errors in prescription, self-medication or overdose.16 These numbers are significant, as DTC advertising increases the probability that people will request medications that advertising convinces them they need.17

Prime Time Pushers Effectively Boosting Profit

Big Pharma operates on profit. In 2018, Open Secrets reported the pharmaceutical industry spent $283.44 million lobbying for their industry.18 In 2016, the health industry spent $29.9 billion on medical marketing, including $20.3 billion on physicians to persuade them of the benefits of their prescription drugs.19

Additionally, in a study published in the Journal of the American Medical Association,20 it was shown that the pharmaceutical industry increased their total spending on DTC from $2.1 billion in 1997 to $9.6 billion in 2016. Of that, $3.45 billion was spent in 2017 on TV ads which increased to $3.7 billion in 2018.21

Money spent on lobbyists and advertising pays off in higher revenues and profit for the pharmaceuticals. Carome believes there are serious downsides to this process. Drug companies advertise the newest medications for which there is the least amount of information about safety,22 and often they hold an exclusive patent.

Although there are older drugs available for the same conditions with a more favorable history of side effects, they are often generic, and the generic industry does not engage in this type of advertising. Safety is the reason the FDA requires a disclosure of risks associated with a drug.

According to Alan Adamson, brand strategy consultant, most of the marketing is aimed at individuals over 65, and an unexpected side effect of compliance with the FDA’s regulation is that it enhances credibility of the advertising.23

Jeff Rothstein24 serves as chief executive officer at CultHealth,25 an ad agency specializing in health care. Rothstein says although it is counterintuitive, they find that when individuals hear about risks it increases their belief in the truthfulness of the whole ad.26

Side Effects Spoken Against Backdrop of Happy Faces

Advertising campaigns used by the pharmaceutical industry may comply to the letter of the law but not the intent. Some have been caught using clever tactics to minimize the risks and overstate the benefits. Risks are mentioned in the ads in a way people do not remember, often listed in small print on the screen or told to the consumer while distracting images play across the television.

One such ad was for Sanofi’s long-acting insulin drug, Toujeo.27,28 Carome ssiad the FDA had warned the company29 about showing distracting images while they discussed alarming side effects.

Once the FDA finds that an ad violates their regulations, they send a warning letter. The ad might be pulled, or it might be reconfigured, but by that time it likely has been on the air for weeks or months and individuals may have been misled.

Bayer was warned about marketing tactics used for their birth control pill Yaz, because their campaign minimized risks and overstated benefits. During the ad,30 side effects were printed on the side of colorful balloons rising into the sky.31 After the warning, Full Measure32 reported Bayer ran a $20 million corrective campaign but was again warned for failing to disclose risks such as heart attack, stroke and death.

In another ad run by Pfizer for the drug Lipitor, Dr. Robert Jarvik, inventor of the artificial heart, talked about his support for it. Jarvik was paid $1.3 million for the ad, which the FDA called misleading. Pfizer pulled the ad.33 Pfizer was also warned about ads for Estring,34 a drug for postmenopausal women, as those ads failed to provide any risk information, including the risk of uterine cancer associated with use of the drug.35

The FDA initially did not agree to an interview, but once Full Measure began investigating, they told the group they were launching a new study about TV commercials, in particular those falling under the disease awareness category.36 The aim was to determine if these ads “may result in consumers misinterpreting and being confused” by the information presented.37

Disease Awareness Ads May Slip Through a Legal Loophole

One example of a disease awareness ad that does not disclose side effects under the current regulations is a vaccine by GlaxoSmithKline for adult whooping cough.38 The ad plays on the Red Riding Hood fairy tale, portraying grandmother as a big bad wolf unintentionally passing along a big bad cough to her darling grandbaby.39

At the conclusion of the ad, they offer a URL to a website where they describe more about the “big bad cough” and how to get vaccinated. If the ad doesn’t mention a brand, it’s considered educational and doesn’t have to mention risks. This is a legal loophole that pharmaceutical companies have used to promote their products.

Merck is yet another pharmaceutical company using the same loophole with its ads for its HPV vaccine.40 Without mentioning its name, Gardasil, the advertisement preys on the guilt a parent may feel in not protecting their teen from cancer spread through sexual contact.

Aside from the fact that Gardasil is not actually a cancer vaccine, but rather a vaccine for a viral infection41 that clears itself in the majority of cases (but can lead to cancer in some cases when a persistent infection is left untreated), the ad does not disclose that the vaccine is associated with blood clots, seizures, motor neuron disease, pancreatitis and paralysis.42

These are the types of ads the FDA is spending tax dollars to “study” in order to determine if the information — or lack of information — is misleading the public.

Michael Sinkinson, assistant professor of economics at Yale School of Management,43 offers a financial perspective on the situation. In his interview with Full Measure, Sinkinson expressed concern that without advertising, drug companies may lose enough revenue and fail to develop new medications:44

“Maybe the math no longer makes sense and you don’t develop the drugs. I think it’s more likely that advertising is the net positive for society for novel drugs, for new treatments and for drugs that are just very cost effective, very effective at keeping you out of the hospital.”

What Has to Happen for Change?

While it may be simple to identify the challenges and obstacles you face from pharmaceutical advertising on television and other media, strategically identifying and executing a plan is more complex. Carome believes45 it’s unlikely we’ll see the demise of these ad campaigns in our lifetime as they are highly profitable for Big Pharma and the media.

Although some believe pharmaceutical companies may lose enough revenue to stop research and development on new drugs, that is how they make money. Once a medication has lost its patent, the company loses exclusive rights to sell the brand name drug and generic copies at a lower cost begin to flood the market.

You may not see a change in advertising on television and other digital media in your lifetime, but you are able to take control by making small changes to improve your health and reduce your dependence on medication. I encourage you to share this newsletter with friends and family so they may discover how to take control of their health, which ultimately impacts daily life and finances.

Simple choices reduce your risk for cardiovascular disease, diabetes, cancer and Alzheimer’s disease, all of which are in the top 10 leading causes of death.46 Here are some of my past articles to help you get started:

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Dsyfunctional Autophagy Promotes Cellular Senescence in Long-Lived Neurons

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Senescent cells cause harm to surrounding tissue when they linger over time, evading the usual fate of self-destruction or destruction by the immune system. They secrete inflammatory and other signals that rouse the immune system into a state of chronic inflammation, destructively remodel nearby tissue, and encourage other cells to become senescent. The presence of senescent cells is a significant cause of aging and age-related disease, as demonstrated by studies in which senolytic therapies are used to selectively remove some portion of the burden of senescent cell in old tissues.

Researchers here show that long-lived non-dividing cells in the brain also become senescent, and that a faltering of the cell maintenance processes of autophagy is important in this process. One of the reasons why autophagy declines with age, particularly in long-lived cells, is the build up of hardy metabolic waste products that clutter the recycling structures called lysosomes, making them inefficient and bloated. More effort should be devoted towards building therapies capable of breaking down the waste products that our biochemistry struggles with.


Senescent cells accumulate in various tissues and organs with aging altering surrounding tissue due to an active secretome, and at least in mice their elimination extends healthy lifespan and ameliorates several chronic diseases. Whether all cell types senesce, including post-mitotic cells, has been poorly described mainly because cellular senescence was defined as a permanent cell cycle arrest. Nevertheless, neurons with features of senescence have been described in old rodent and human brains.

In this study we characterized an in vitro model useful to study the molecular basis of senescence of primary rat cortical cells that recapitulates senescent features described in brain aging. We found that in long-term cultures, rat primary cortical neurons displayed features of cellular senescence before glial cells did, and developed a functional senescence-associated secretory phenotype able to induce paracrine premature senescence of mouse embryonic fibroblasts but proliferation of rat glial cells.

Functional autophagy seems to prevent neuronal senescence, as we observed an autophagic flux reduction in senescent neurons both in vitro and in vivo, and autophagy impairment induced cortical cell senescence while autophagy stimulation inhibited it. Our findings suggest that aging-associated dysfunctional autophagy contributes to senescence transition also in neuronal cells.

Link: https://doi.org/10.18632/aging.102181

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Upregulation of Autophagy Reverses Age-Related Decline of Memory B Cell Function

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Memory B cells undertake some of the more important tasks in coordination of an effective immune response, circulating in the body to accelerate the deployment of other resources in the immune system to tackle a specific threat. Dysfunction in B cells is a significant component of the onset of age-related immunosenescence, the progressively greater incapacity of the immune system. Selectively removing and replacing B cells has been shown to improve matters, but here researchers identify failing autophagy as an important factor. B cells are long-lived, and long-lived cells tend to build up metabolic waste that is resilient to the enzymes available to break it down. This gums up the structures and systems used in autophagy, causing it to fail, and the cells to thus become ever more cluttered with damaged protein machinery and other harmful waste. This in turn degrades function.


During a regular influenza season, about 90% of the deaths occur in people older than 65 years. Immune responses to vaccines are known to be particularly ineffective in the elderly population. A major correlate of protection for vaccinations is the specific antibody titer generated by long-lived plasma B cells. With a lifespan of several decades, long-lived lymphocytes are particularly prone to accumulation of intracellular waste. Autophagy recycles unwanted cytoplasmic material. Autophagy-deficient lymphocytes are unable to generate adequate responses, in particular long-lived lymphocytes, memory T cells, memory B cells, and plasma B cells.

Here we show that reduced autophagy is a central molecular mechanism underlying immune senescence. Autophagy levels are specifically reduced in mature lymphocytes, leading to compromised memory B cell responses in old individuals. Spermidine, an endogenous polyamine metabolite, induces autophagy in vivo and rejuvenates memory B cell responses. Mechanistically, spermidine post-translationally modifies the translation factor eIF5A, which is essential for the synthesis of the autophagy transcription factor TFEB. Spermidine is depleted in the elderly, leading to reduced TFEB expression and autophagy. Spermidine supplementation restored this pathway and improved the responses of old human B cells. Taken together, our results reveal an unexpected autophagy regulatory mechanism mediated by eIF5A at the translational level, which can be harnessed to reverse immune senescence in humans.

Link: https://doi.org/10.1016/j.molcel.2019.08.005

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Lower LDL Cholesterol and Blood Pressure Over a Lifetime Correlate with Greatly Reduced Risk of Cardiovascular Disease

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Numerous genetic variants correlate with either lower LDL cholesterol or lower blood pressure. Some of these have been shown to result in greatly reduced risk of cardiovascular disease, such as variants in APOB, DSCAML1, ANGPTL4, and ASGR1. Researchers here adopt the position that one can use data on the health of individuals with these and other variants from a large population database as a way to model the outcome should a non-variant individual diligently control LDL cholesterol and blood pressure through lifestyle choices throughout life. This is probably a fair assumption, though it is also fair to suggest that not all of the relevant mechanisms touched on by these genetic variants are fully understood.

As one might expect, based on the results from earlier studies of specific variants and risk of cardiovascular disease, the data here shows a large reduction in risk for people who have one or more of these variants. This can then be associated with the level of reduction in LDL cholesterol and blood pressure needed for a non-variant individual to achieve the same outcome. Assuming, of course, that cholesterol levels and blood pressure are the only relevant mechanisms, or at least the dominant mechanisms. They are undoubtedly influential, given that higher LDL cholesterol accelerates atherosclerosis and higher blood pressure results in all sorts of tissue damage, but they are not the only influential processes in aging.

A life of low cholesterol and BP slashes heart and circulatory disease risk


In this study, researchers studied 438,952 participants in the UK Biobank, who had a total of 24,980 major coronary events – defined as the first occurrence of non-fatal heart attack, ischaemic stroke, or death due to coronary heart disease. They used an approach called Mendelian randomisation, which uses naturally occurring genetic differences to randomly divide the participants into groups, mimicking the effects of running a clinical trial.

People with genes associated with lower blood pressure, lower LDL cholesterol, and a combination of both were put into different groups, and compared against those without these genetic associations. Differences in blood LDL cholesterol and systolic blood pressure (the highest level that blood pressure reaches when the heart contracts), along with the number of cardiovascular events was compared between groups.

A long-term reduction of 1 mmol/L low-density lipoprotein (LDL), or ‘bad’ cholesterol, in the blood with a 10 mmHg reduction in blood pressure led to an 80 percent lower lifetime risk of developing heart and circulatory disease. This combination also reduced the risk of death from these conditions by 67 percent. The team found that even small reductions can provide health benefits. A decrease of 0.3 mmol/L LDL cholesterol in the blood and 3 mmHg lower blood pressure was associated with a 50 percent lower lifetime risk of heart and circulatory disease.

Association of Genetic Variants Related to Combined Exposure to Lower Low-Density Lipoproteins and Lower Systolic Blood Pressure With Lifetime Risk of Cardiovascular Disease


Numerous randomized trials have demonstrated that treatment for up to 5 years with therapies that reduce low-density lipoprotein cholesterol (LDL-C) and systolic blood pressure (SBP) reduce the risk of cardiovascular events. In addition, mendelian randomization studies suggest that the benefit of exposure to lower LDL-C levels and lower SBP may accumulate over time. Because the biological effects of LDL-C and SBP may be cumulative, long-term exposure to the combination of both could potentially substantially reduce the lifetime risk of cardiovascular disease. However, the association of combined lifetime exposure to both lower LDL-C and lower SBP with the risk of cardiovascular disease has not been reliably quantified.

Ideally, this question would be addressed by conducting a randomized trial to minimize the effect of confounding that can occur in observational studies. However, a randomized trial evaluating the association between maintaining prolonged exposure to both lower LDL-C levels and lower SBP with the risk of cardiovascular disease would take several decades to complete, and therefore is unlikely to ever be conducted.

In an attempt to fill this evidence gap, this study used genetic variants associated with lower LDL-C levels and SBP as instruments of randomization to divide participants into groups with lifelong exposure to lower LDL-C levels, lower SBP, or both; and then compared the differences in plasma LDL-C, SBP, and cardiovascular event rates in each group to estimate the association of combined lifetime exposure with the lifetime risk of cardiovascular disease in a manner analogous to a long-term randomized clinical trial. The primary objective of this study was to assess and quantify the association of prolonged exposure to the combination of both lower LDL-C and lower SBP with the lifetime risk of cardiovascular disease.

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Intervene Immune Publishes Thymus Regrowth Trial Results

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Intervene Immune is the company formed to commercialize the methology for regrowth of thymic tissue used in the small TRIIM (Thymus Regeneration, Immunorestoration, and Insulin Mitigation) trial, a combination of growth hormone, DHEA, and metformin. As I’ve noted in the past, that the approach involves the use of human growth hormone over an extended period of time makes it less desirable as an intervention, but if one can gain an expectation of some thymic regeneration, leading to an extended improvement in immune function that lasts for years beyond the treatment period, then it might be worth the trade-off. In general, higher growth hormone levels are associated with a worse outcome in the study of aging, while lower levels are associated with a slowing of aging. Using growth hormone for anything other than treating rare clinical conditions of deficiency is something like burning the candle at both ends.

The thymus is an inaccessible organ in the chest responsible for transforming thymocytes created in the bone marrow into T cells of the adaptive immune system. This complicated process takes place in thymic tissue that, unfortunately, atrophies with age, becoming replaced with fat. The less tissue, the fewer T cells are generated, and the worse the function of the immune system over time. The thymus loses much of its mass quite early in life, following childhood, but the later, slower decline over the course of adult life is a different process mediated by chronic inflammation and other factors that arise with old age. The adaptive immune system is vital to health, and thus a great deal of research has taken place over the past few decades into means of thymic regeneration: upregulation of FOXN1 or related genes such as BMP4; engineering of new thymic tissue; delivery of recombinant KGF, delivery of growth hormone; sex steroid ablation; and so forth. Some are more reliable than others, and some, such as KGF, have succeeded in mice and failed in human trials.

The Intervene Immune team has presented a fair amount of data on the results from their trial at recent conferences, including epigenetic age changes, and you’ll find it all in the open access paper noted here. The results unfortunately don’t include all of the assays of immune cell characteristics one might want in order to be able to compare directly with the effects of sex steroid ablation in human patients, but are intriguing. (In turn the sex steroid ablation trials didn’t look at thymic mass in CT scans, an unfortunate omission). Further, it isn’t possible to clearly associate all of the outcomes with regrowth of thymic tissue, particularly the epigenetic age effects, given everything else the treatment might be doing. Nonetheless, taken as a whole this is good supporting evidence for those groups working on more direct approaches to the problem of the atrophied thymus, such as Lygenesis and the company Bill Cherman and I founded last year, Repair Biotechnologies.

First hint that body’s ‘biological age’ can be reversed


A small clinical study has suggested for the first time that it might be possible to reverse the body’s epigenetic clock, which measures a person’s biological age. For one year, nine healthy volunteers took a cocktail of three common drugs – growth hormone and two diabetes medications – and on average shed 2.5 years of their biological ages, measured by analysing marks on a person’s genomes. The participants’ immune systems also showed signs of rejuvenation.

The latest trial was designed mainly to test whether growth hormone could be used safely in humans to restore tissue in the thymus gland. The gland, which is in the chest between the lungs and the breastbone, is crucial for efficient immune function. White blood cells are produced in bone marrow and then mature inside the thymus, where they become specialized T cells that help the body to fight infections and cancers. But the gland starts to shrink after puberty and increasingly becomes clogged with fat. Evidence from animal and some human studies shows that growth hormone stimulates regeneration of the thymus. But this hormone can also promote diabetes, so the trial included two widely used anti-diabetic drugs, dehydroepiandrosterone (DHEA) and metformin, in the treatment cocktail.

Checking the effect of the drugs on the participants’ epigenetic clocks was an afterthought. The clinical study had finished when researchers conducted an analysis. Four different epigenetic clocks were used to assess each patient’s biological age, and he found significant reversal for each trial participant in all of the tests. “This told me that the biological effect of the treatment was robust. The effect persisted in the six participants who provided a final blood sample six months after stopping the trial. Because we could follow the changes within each individual, and because the effect was so very strong in each of them, I am optimistic,”

Reversal of epigenetic aging and immunosenescent trends in humans


Thymus regeneration and reactivation by growth hormone administration have been established in aging rats and dogs by restoration of youthful thymic histology and by reversal of age-related immune deficits. The present study now establishes highly significant evidence of thymic regeneration in normal aging men accompanied by improvements in a variety of disease risk factors and age-related immunological parameters as well as significant correlations between thymic fat-free fraction (TFFF) and favorable changes in monocyte percentages and the lymphocyte-to-monocyte ratio (LMR), independent of age up to the age of 65 at the onset of treatment. These observations are consistent with the known ability of growth hormone to stimulate hematopoiesis and thymic epithelial cell proliferation. Our finding of an increase in FGF-21 levels after 12 months of treatment suggests that thymic regeneration by the present treatment may be mediated in part by this cytokine, which we believe is a novel finding.

Treatment-induced increases in naïve CD4 and naïve CD8 T cells were relatively small compared to changes reported in recombinant growth hormone treated HIV patients, but our volunteer population was pre-immunosenescent and not depleted of naïve CD4 and naïve CD8 T cells at baseline. Positive responses also occurred despite potential complications caused by lymph node aging. Therefore, the small increases observed in these cells and in CD4 T-cell recent thymic emigrants are consistent with the ultimate goal of preventing or reversing the normal age-related collapse of the TCR repertoire at ages just above those of our study population.

There may be both immunological and non-immunological mechanisms of epigenetic aging reversal. Growth hormone, DHEA, and metformin have unique effects that are in opposition to aging, and it is possible that the specific combination of these agents activates a broad enough range of therapeutic pathways to account for the previously unpredictable reversal of epigenetic aging, even independently of the immunological markers we have measured.

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