3-D bioprinting is a form of rapid prototyping adapted to the tissue engineering industry. Printers assemble tissues from ink containing cells and supporting materials of various types. Given a suitable recipe, the result is a functional tissue quite close to the real thing in structure and function. The interesting part of this open access paper is not that the team bioprinted small-scale model hearts as their proof of concept, given that these are not fully functional heart tissues capable of the electrical coordination required to exhibit a heart beat, and nor is it that they used materials personalized to a specific patient. Rather, it is that they demonstrate the ability to bioprint networks of small blood vessels sufficient to support the interior cells of a thick tissue.
This is an important advance, even given that it is not the full microvascular networks of capillaries found in natural tissue. This matter of blood vessels is a major challenge in the tissue engineering community. Cells need a supply of blood in order to survive, and that supply must be carried by blood vessels for any distance much over a millimeter. Finding a reliable way to incorporate blood vessel networks into tissues is the primary roadblock holding back construction of replacement organs, and it is why so much work today is focused on the production of tiny, thin organoid tissue sections.
Generation of thick vascularized tissues that fully match the patient still remains an unmet challenge in cardiac tissue engineering. Here, a simple approach to 3D-print thick, vascularized, and perfusable cardiac patches that completely match the immunological, cellular, biochemical, and anatomical properties of the patient is reported. To this end, a biopsy of an omental tissue is taken from patients. While the cells are reprogrammed to become pluripotentstem cells, and differentiated to cardiomyocytes and endothelial cells, the extracellular matrix is processed into a personalized hydrogel. Following, the two cell types are separately combined with hydrogels to form bioinks for the parenchymal cardiac tissue and blood vessels.
In recent years, the strategy of 3D tissue printing evolved, allowing the creation of vasculature within hydrogels. However, in most of the studies, the endothelial cells (ECs) that form the blood vessels were printed without the parenchymal tissue, which was later on casted on top of the vessels. In other pioneering works, the researchers were able to print ECs together with thin surrounding tissues. However, the obtained tissues were not thick, the ECs did not form open blood vessels and perfusion through them was not demonstrated. Different strategies include printing of the parenchymal tissue with open, a-cellular channels in between, followed by external perfusion of ECs to form the blood vessels. Finally, decellularized hydrogels were also used for printing nonvascularized tissues. Therefore, to the best of our knowledge, the aforementioned studies did not demonstrate printing of a full, thick vascularized patch in one step.
Here, we report on the development and application of advanced 3D printing techniques using the personalized hydrogel as a bioink. In this strategy, when combined with the patient’s own cells, the hydrogel may be used to print thick, vascularized, and perfusable cardiac patches that fully match the immunological, biochemical and anatomical properties of the patient. Furthermore, we demonstrate that the personalized hydrogel can be used to print volumetric, freestanding, cellular structures, including whole hearts with their major blood vessels
You know that feeling of energy and productivity you get after finishing your morning’s first cup of coffee? It turns out you can get that without even drinking a drop, just by thinking about coffee.
The provocative finding not only highlights the power of thought but also suggests you may be able to get a boost just from thinking about your favorite brew — a habit that may benefit those who drink coffee too close to bedtime. To be clear, organic black coffee can be quite healthy, but for those looking to abstain (such as during pregnancy), your alertness needn’t suffer — just think about pouring yourself a cup.
Thinking About Coffee Arouses Your Brain
In a study involving people from both Western and Eastern cultures, researchers from the University of Toronto’s Rotman School of Management exposed participants to coffee- and tea-related cues in a series of studies.1 Lead author Sam Maglio said in a news release:2
“People often encounter coffee-related cues, or think about coffee, without actually ingesting it … We wanted to see if there was an association between coffee and arousal such that if we simply exposed people to coffee-related cues, their physiological arousal would increase, as it would if they had actually drank coffee.”
While a lot is known about the physiological effects of coffee and caffeine on the body, the researchers explained, less is known about its psychological effects. However, it appears that many people’s brains may be primed toward arousal at the very thought of coffee, especially in Western cultures, where coffee dominates over tea.
After being exposed to coffee-related cues, such as images of coffee, the study participants perceived time as shorter and thought in more concrete, precise terms, which is suggestive of a more alert state of mind.
“People who experience physiological arousal – again, in this case as the result of priming and not drinking coffee itself — see the world in more specific, detailed terms. This has a number of implications for how people process information and make judgments and decisions,” Maglio said.3
The effects were stronger among Westerners than those in Eastern cultures, perhaps because the West maintains a stronger association between coffee and alertness. “In North America we have this image of a prototypical executive rushing off to an important meeting with a triple espresso in their hand,” Maglio continued. “There’s this connection between drinking caffeine and arousal that may not exist in other cultures.”4
Smelling Coffee Increases Alertness Too
Many people love to wake up to the scent of coffee, and it seems this, too, may be one way to jump-start your day — and your brain. Researchers had university students take GMAT algebra tests in a computer lab with an ambient coffee-like scent or no scent. Those in the coffee-scented room performed better on analytical reasoning tasks.5
The researchers also did a follow-up survey asking whether participants believed they would perform better in a room scented with coffee or flowers or no scent at all. Most believed the coffee-scented room would boost their performance, and this expectation, the researchers concluded, was partly responsible for the improved performance shown during testing.
“Our results thus demonstrate that a coffee-like scent (which actually contains no caffeine) can elicit a placebo effect,” the study noted.6 The findings lend even more support to the notion that keeping a bag of coffee beans on hand for a quick whiff could you give you a mental boost in a pinch — no coffee drinking required.
The Case for Drinking Coffee
Coffee is one of the most consumed beverages in the world, and it’s intriguing that the love for coffee runs so deep that it may exert effects via scent or suggestion. However, the case can be made that drinking coffee is a good habit to get into, as it’s been linked to decreased mortality from a number of diseases, including heart disease, neurological diseases, Type 2 diabetes and several types of cancer, including endometrial and liver.7
There are more than 800 volatile compounds in coffee, although caffeine and chlorogenic acids are the most common. While it was long suggested that coffee consumption could be harmful, it’s now generally believed that moderate amounts of coffee (three to four cups) have few health risks and much evidence of health benefits.8
In one review of 112 meta-analyses about coffee, this popular beverage was linked to a probable decreased risk of colorectal, colon, endometrial and prostate cancers, cardiovascular disease and mortality and Parkinson’s disease, with researchers noting, “Given the spectrum of conditions studied and the robustness of many of the results, these findings indicate that coffee can be part of a healthful diet.”9
As far as your brain is concerned, drinking coffee is known to boost alertness, well-being and concentration, along with improving mood and reducing depression. While it can potentially disrupt your sleep, particularly if you drink it at night, and may increase anxiety in certain people, coffee is linked to a host of brain benefits, including:10
Prevention of cognitive decline
Reduced risk of stroke
Lower risk of Alzheimer’s disease
Coffee May Be Even Better if You’re Over 45
The benefits of drinking coffee may only get better with age — a major positive, since for many the love for coffee is lifelong. In fact, a 10-year study presented at the European Society of Cardiology congress in Barcelona showed that people who drank four cups of coffee per day had a 64% decrease in their risk of dying from any cause.
Among those aged 45 and over, however, every two cups of daily coffee lowered the risk of dying during the study period by 30%; no such association was seen in younger adults.11
In another study, this one in individuals aged 60 years and older, drinking two or more cups of coffee a day was associated with a lower risk of impaired agility in women and in those with obesity. Consuming two or more cups of coffee a day was also associated with a lower risk of impaired mobility in women.12
Coffee may also have a protective effect as you age, including in the case of silent brain infarction (SBI), which are often found in brain scans in healthy elderly people and may be associated with dementia and cognitive decline. Compared with those who didn’t drink coffee, people who drank three or more cups of coffee a day during middle age had a lower incidence of SBI.
“Our report demonstrated that SBI was observed less frequently in middle aged Japanese who consumed 3 cups or more of coffee per day. To avoid senile dementia and/or symptomatic infarction in older age, the middle-aged individuals might have to drink more than 3 cups of coffee every day,” researchers wrote in the Journal of Stroke and Cerebrovascular Diseases.13
Drinking two to four cups of caffeinated coffee daily has even been associated with a 50% reduced suicide risk among adults, compared to drinking one cup or less of caffeinated coffee, or decaf.14
Protect Your Heart With Coffee?
There are many heart-healthy actions you can take, from eating right to exercising — but is drinking coffee among them? It turns out that even your heart can benefit from a cup of joe.
Research presented at the American Heart Association’s Scientific Sessions 2017 found, for instance, that compared to non-coffee drinkers, coffee drinkers had a 7 percent lower risk of heart failure and an 8 percent lower risk of stroke for each additional cup of coffee consumed per week.15
Drinking more than three cups of coffee a day may also lower your risk of developing atherosclerosis, also known as clogged arteries, a condition that seriously increases your heart disease risk, by 63%, particularly in people who have never smoked.
“Based on our results and prior studies, consumption of coffee could exert a potential beneficial effect against coronary calcification and cardiovascular disease risk, particularly in nonsmokers,” researchers wrote in the Journal of the American Heart Association. “It is possible that deleterious effects of smoking overwhelm the benefits of coffee intake on early cardiovascular disease injury, so this impact of coffee may occur only in people who have never smoked.”16
Coffee Contains Antioxidants
When you think of antioxidants, you may think mostly about fruits and vegetables, but coffee is another excellent source. Further, because coffee is so widely consumed, it’s considered to be a major contributor to dietary antioxidants. With each sip, you’re gaining these beneficial compounds that can scavenge free radicals and more, as researchers explained in Molecules:17
“Brewed coffee is a complex food matrix with numerous phytochemical components that have antioxidant activity capable of scavenging free radicals, donating hydrogen and electrons, providing reducing activity and also acting as metal ion pro-oxidant chelators.
More recent studies have shown that coffee components can trigger tissue antioxidant gene expression and protect against gastrointestinal oxidative stress.”
While many of the benefits of coffee, including its cognitive ones, are often attributed to caffeine, research has shown similar benefits, including increased alertness, leading researchers to speculate that there may be other properties in coffee responsible for its psychoactive effects.18
What’s the Healthiest Type of Coffee?
If you’re not a coffee drinker, there’s no reason to feel compelled to start. There are still many other dietary additions you can make to naturally ward off disease and improve your health. However, if you enjoy coffee, there’s good reason to savor a cup — or a few — each day, though there are some caveats to consider.
Coffee, which is a heavily pesticide-sprayed crop, should always be organic, as well as shade-grown. Coffee is a shade-loving plant, but growers often strip forests to make growing and harvesting easier. This destroys the ecological habitat of many natural pest deterrents, such as birds and lizards, while the pests flourish, resulting in additional pesticide use in nonshade-grown varieties.
Drink your coffee black, skipping the added sugar and milk or cream, as the antioxidant capacity of coffee may be significantly decreased by the addition of milk.19 If you want to add something to your coffee, try coconut oil or medium-chain triglyceride (MCT) oil, which may help you burn fat and improve mitochondrial function.
Start with a small amount, such as 1 teaspoon of MCT oil, working your way up to 1 or 2 tablespoons, to avoid gastrointestinal side effects. You can also blend in a pat of raw grass fed butter. This recipe is a favorite among those following a ketogenic diet.
Finally, while most people can safely consume coffee, if you’re pregnant you should avoid it due to the caffeine. Coffee consumption during pregnancy has been linked to low birth weight babies,20 heart problems21 and behavioral disorders in later life,22 so this is one population who can benefit instead by just thinking about, or smelling, this popular brew.
The Life Extension Advocacy Foundation (LEAF) volunteers were at the recent Undoing Aging conference in Berlin, and spent much of their time interviewing a selection of the attending scientists and entrepreneurs. The interviews are being published at the LEAF blog as they are made ready, and here I’ll point out the latest. The research and development communities focused on treating aging are becoming very diverse. A wide range of activities are underway, driven by an equally wide range of views on the nature of aging and where best to intervene. Most work at the present time, well represented in these interviews, involves upregulation of stress responses, attempts to encourage greater stem cell activity, reduction in chronic inflammation, greater mitochondrial function, and other forms of overriding the regulation of aged metabolism, forcing it into a modestly better state.
As regular readers well know, I am strongly in favor of an alternative strategy, meaning a focus on the damage that causes aging. Striking as close to the root of aging as possible is the best path forward. That damage must either be repaired or made irrelevant, whichever of those two options turns out to be easier and faster in each specific case. If damage is removed, then the operation of metabolism will largely take care of itself. This should also be less challenging than any other approach: there are comparatively few root causes of aging and comparatively many downstream issues. Further, the causes are largely less complex than the forms of dysfunction and disease that result. Nonetheless, most present medical development initiatives attempt to compensate for the downstream issues of aging, and are thus both expensive and largely ineffective in the grand scheme of things. We need to do better than this if we are to live to see meaningful extension of healthy human life spans.
One of the challenges in the aging space is that the kind of underlying discovery work that usually drives translational pipelines is really lacking, because the space is just so new. If you’re looking at molecular targets of cardiovascular disease, cancer, or things like that, a lot of these targets have been thoroughly vetted by academic institutions in the peer-reviewed literature, and you have some level of confidence that the thing that you’re going after is actually an appropriate target. But, because the aging space is so new, there’s lots of new targets that are being discovered, but there hasn’t really been enough time for academia to properly vet those targets. Some of them are very good real targets that we should be going after, and others are artifacts and might not actually be real or as impactful as we think.
So, at Ichor, we started doing, a while ago, a lot of contract work to try to help other companies that need to bring industrial-grade rigor to basic science and to early discovery and then move from that early-stage discovery work into full-on development programs, which are more akin to a traditional pharmaceutical pipeline. That contract work has grown; we’ve helped a lot of companies and worked with a lot of clients, and we’ve run into a need to have dedicated teams for project management and really making sure that all of the client projects get plugged into the pipeline to get our best efforts and everything else, and that’s where Huda’s coming in and spinning out all of our contract research into Icaria Life Sciences.
Why is Alkahest focusing on plasma proteins as a promising area for rejuvenation therapies?
Our founding science demonstrated that there are certain proteins present in plasma that can confer effects on biological function in aging. Their relation to the processes of aging is supported by the observation that many of these functional proteins increase or decrease with age – we have termed these functional plasma proteins chronokines. There are beneficial chronokines known to decline with age that we can increase and thus delay the onset of aging-related disorders, and there are detrimental chronokines which increase with age that we can inhibit for this purpose. We have therefore focused on deeply understanding the plasma proteome as a source of therapies, both plasma-based and traditional pharmaceutical modalities like small molecule inhibition.
Why use rapalogs rather than just rapamycin? Is there actually good data showing that rapamycin in moderate doses is harmful to humans?
Our lead program is determining if TORC1 inhibition improves the function of the aging immune system and thereby decreases the incidence of respiratory tract infections (RTIs) in elderly humans. In a Phase 2a clinical trial, we found that RTB101, a catalytic site mTOR inhibitor (not a rapalog), led to a greater reduction in infection rates than the rapalog everolimus. We used very low doses of both RTB101 and everolimus in this trial, and both drugs were safe and well tolerated at these low doses.
When do you anticipate finishing clinical trials and being able to offer commercially available therapies for RTIs and other diseases that resTORbio is targeting?
We anticipate finishing two Phase 3 clinical trials, which will determine if RTB101 decreases the incidence of respiratory illness in people age 65 and older, in 2020. If the Phase 3 trials are successful, we anticipate submitting a New Drug Application.
What do you think is the best method of measuring telomeres?
We call the most sensitive assay TeSLA, for telomere shortest length assay. Most scientists use a qPCR assay that is not very reliable but easy to use. It is well established that it is the shortest telomeres that leads to replicative senescence. There are thousands of published papers using the qPCR making extraordinary claims based on very small differences in average telomere length. Other methods include TRF and Q-FISH, and these are intermediate in their ability to see some but not all the shortest telomeres.
What are your thoughts on restoring telomere length using transient telomerase induction as a therapeutic approach to aging?
It is a reasonable idea, and we are currently doing such experiments. Initially, it will be done ex vivo, e.g. in the cell culture lab, to prove it works and does no harm. We can then give individuals back their own cells, potentially with slightly elongated telomeres.
Read nore about N . O . and Heart health and fitness.
Regular physical exercise acts to slow the characteristic loss of muscle mass and strength that occurs with aging, a condition known as sarcopenia once it reaches the point of frailty. In this, strength training appears to work more effectively than aerobic exercise, but both have their place in the overall picture. In the paper here, researchers report on their assessment of proteomic changes with both aging and exercise. They find that, much as expected, the changes in protein levels that occur with age are largely opposed by the changes in protein levels caused by physical activity.
The decline in muscle strength is one of the most striking phenotypes of aging, which is only partially accounted for by a reduction in muscle mass, suggesting a loss of cellular and molecular integrity of muscle tissue, and/or impairment of neuromuscular control with aging. Low muscle strength is a powerful, independent predictor of slow gait, mobility disability, and early mortality. No interventions are currently available that can prevent or attenuate the decline in muscle strength with aging except exercise, especially resistance training. In spite of this evidence, the percentage of people who regularly exercise is still low and this percentage declines with aging.
It has been suggested that people who have an active lifestyle in daily life have a slower decline of muscle mass and strength with aging. Understanding how physical activity in daily life affects muscle physiology in older persons might help in developing new interventions that, by targeting the same mechanisms triggered by physical activity, could prevent the development of muscle impairment with aging. Numerous studies have investigated the impact of a sedentary lifestyle and low physical activity on health outcomes in both younger and older individuals. Physical inactivity, either long or short-term, negatively affects muscle performance and is associated with diminished aerobic capacity, as well as reduced insulin sensitivity and basal metabolic rate. Furthermore, physical activity alone has been shown to improve and regulate metabolic homeostasis and metabolic efficiency.
Overall, an active lifestyle could be conceptualized as a mixture of aerobic and resistance exercise, but the intermittent, and variable mixture of these activities make it difficult to study. Endurance and resistance training elicit both common and specific metabolic/morphologic adaptations in muscle, some of which are common between tissues. In general, the stress that is induced by exercise challenges energy homeostasis in myocytes, shifting the cellular environment towards an oxidative state. This induces microdamage that stimulates both transcriptional and posttranscriptional responses, which then promotes synthesis of specific proteins that seek to reestablish a different homeostatic equilibrium. Endurance training maximally stimulates mitochondrial biogenesis, enhances aerobic metabolism and fatty acid utilization, and produces change in muscle fiber composition. In contrast, heavy resistance training stimulates the synthesis of contractile proteins, leading to muscle hypertrophy, and increases in maximal contractile force speed and output. Whether an active lifestyle is sufficient to activate the same biological mechanisms triggered by endurance and resistance training is unknown.
In recent years, a handful of studies have examined the protein composition of human muscle cell types and tissues including proteomic differences between old and young muscle, athletes and non-athletes, exercise in extreme conditions, and physical activity and metabolic disorders. These studies have helped to characterize the physiological adaptations of healthy human muscle to different types of exercise. Most of these studies focused on the acute and immediate effects of short bouts of high intensity exercise in either human or mice/rat models, as well as long-term effects of exercise. However, very little research has focused on assessing the association of daily physical activity with the muscle proteome in healthy community-dwelling individuals.
To verify whether an active lifestyle is associated with detectable changes in skeletal muscle and to start to characterize these changes, we performed a quantitative, mass spectrometry-based proteome analysis of muscle specimens from a group of well-characterized healthy individuals with a wide age-range (20-87 years) and who self-reported different levels of physical activity. Independent of age and technical covariates, we found that high levels of physical activity (versus low levels) were associated with an overrepresentation of mitochondrial proteins, tricarboxylic acid (TCA) cycleenzymes, chaperone proteins, and proteins associated with genome maintenance. In contrast, proteins related to the spliceosome and transcription regulation, immune proteins, apoptosis proteins, DNA damage proteins, and senescent proteins were underrepresented in muscle of participants who reported higher physical activity. Differences observed were mostly opposite to those observed with skeletal muscle aging.
There is no shortage of theorizing on the nature of aging: its biochemical causes; its evolutionary origins; how it progresses; how to measure it. In any era in which thinking is cheap and life science research is expensive, there will be a lot more theorizing than data. While the tools of biotechnology cost less than ever, and the price continues to fall even as capabilities increase radically, I think it arguably the case that we are still in the era of relatively cheap thought and relatively expensive research.
One area in which theory and modeling has over the years found its way to practical use in clinical medicine is in the construction of measures of aging based on a straightforward combination of measures, such as grip strength, markers of inflammation, and so forth. Geriatric medicine has and continues to make widespread use of these assessments of frailty. A great deal of work on measures of aging still takes place, as illustrated by the growth of epigenetic clocks on the one hand and more complex algorithmic combinations of simple health metrics on the other. The work here is an example of the latter, with the choice of metrics and their combination driven by a systems biology view of aging.
Even to the untrained eye it has always been apparent that different people age differently. Subjective evaluation of age rather accurately assesses the ravages of time and coincides quite adequately to more objective metrics. Nevertheless, we would like to be able to reference such objective measures to examine in greater detail the dimensions of aging. The dimensions of aging encompass at least three different aspects. The first incorporates prediction of survival or mortality. In other words, we want to be able to relate a process, aging, to an outcome, longevity. This has long been a domain of aging research, and it continues to engage biodemographers. The second attempts to relate an aging process to the ability to function. So-called healthy aging derives from this approach. Finally, the need to evaluate potential therapies or interventions to extend this healthspan is yet another dimension.
Deficit indices, also known as frailty indices, constitute an uncomplicated way in which to describe the behavior of a complex aging system. Deficit indices have a long history in human aging research and in geriatrics. A deficit index is constructed from a number of signs, symptoms, marks, and manifestations. The number can be relatively small, about twenty, or much larger, as long as it is statistically sufficient. These deficits should encompass many different body or physiological systems. The deficit index arises by summing the deficits counted and dividing by the total number of deficits assessed. Increasing the number of deficits scored improves deficit index performance.
Recently, the deficit index has acquired a strong theoretical underpinning. The deficits are represented by the components of a network, in which they can be damaged or undamaged (deficits per se). By definition, the components are connected by edges. Some of them have more edges than others, performing a more critical role in the network. Damage in this network, whether partial or complete, is propagated across the network or system because of the edges. This rational, systems biology-based nature of the deficit index distinguishes it from other quantitative measures of biological age. In addition, the deficit index is uncomplicated mathematically, as opposed to most of the other measures, and it predicts mortality without the incorporation of chronological age as one of its items.
We have constructed a deficit index we call frailty index-34 (FI34), consisting of 34 health and function variables. The reference to frailty in the name stresses the relevance of the index as a measure of relative health. FI34 is a good predictor of mortality, so it is a measure of biological age. It increases exponentially with calendar age, as we would expect of a predictor of mortality. Moreover, it distinguishes different patterns of aging, and it is heritable. FI34 also captures the individual variability or heterogeneity of aging among individuals. Although constantly increasing with chronological age across a population, it shows variation among individuals in cross-section and longitudinally.
Warning: This oil comes with potentially damaging side effects due to the ingredient it’s made from or the manufacturing process used to extract it. Because these negative effects overshadow the potential benefits, I do not recommend this oil for therapeutic use. Always be aware of the potential side effects of any herbal oil before using.
Among the many crops grown in the United States is cotton. According to the National Cotton Council, roughly 162 pounds of cottonseed are produced for every 100 pounds of fiber.1
The raw cottonseed actually consists of three commodities: linters, which are cotton fibers still clinging to the harvested seeds and which are used to make a variety of products, from paper money to cosmetics to photography film; the hulls, which are pressed into a meal or used as a bulk food in the livestock feed industry; and the kernels inside the hulls, which are crushed to produce the oil.2
As an agriculture product in the U.S., cottonseed oil is considered to be “one of the country’s most important sources for vegetable oil,” according to the Agricultural Marketing Resource Center.3 While cottonseed oil is also touted by the industry to be “cholesterol-free with a high level of antioxidants,” making it a “premium oil” for cooking, baking and use by the processed (snack) food industry,4 fine food magazines such as Bon Appetit warn that it’s one of the top three “least healthy” oils for you.5
This is one reason why I would not recommend it as part of your diet. Before I explain my stand, here is what mainstream recommendations say about this vegetable oil.
What Is Cottonseed Oil?
Cottonseed oil is a fairly common vegetable oil in the U.S. and was used as early as the 1800s.6 It was called “America’s original vegetable oil” and created a high demand among its consumers.7 Cottonseed oil is similar to canola, corn, safflower, soybean and sunflower in terms of its polyunsaturated fat oil composition.8 In its nonhydrogenated form, it can be used for deep frying to lower the amounts of trans fat in fried foods.9
Uses of Cottonseed Oil
Cottonseed oil is known for its culinary purposes. It’s used for frying or baking, and added to salad dressings,10 baked goods, cereals and mayonnaise.11 Because of its neutral taste, cottonseed oil will not mask or overpower the other flavors in your dish, unlike other oils.12 It’s a familiar feature of processed foods,13 like potato chips14 and French fries,15 which I absolutely recommend you avoid if you want to achieve optimal health.
Cottonseed oil is added to margarines, icings and whipped toppings because of its potential to help form beta prime crystal, which gives these food products a smooth and creamy appearance and consistency.16
Cottonseed oil is also added to personal care products such as soap and cosmetics,17 lubricants, nail polish removers, fertilizers18 and laundry detergents.19 This oil is even added to soaps used in washing wool. In the first half of the 20th century, cottonseed oil was also used as an excipient in drugs like penicillin and vaccines, but was replaced by peanut oil after cotton seed allergy reactions began being reported.20
Today cottonseed oil is one of many used as emulsifiers and excipients approved for use in a range of drugs and vaccines.21,22
Composition of Cottonseed Oil
Cottonseed oil is mainly composed of polyunsaturated fatty acids (PUFAs), with linoleic acid making up a majority of its PUFA content.23 Other fatty acids that can be found in cottonseed oil include palmitic acid, myristic acid, palmitoleic acid, stearic acid, oleic acid and linolenic acid. The fatty acid composition of nonhydrogenated cottonseed oil is:24
Saturated fat — 27%
Monounsaturated fat — 18%
Polyunsaturated fat — 55%
When partially hydrogenated, cottonseed oil’s fatty acid profile is altered and its monounsaturated fatty acid (MUFA) concentrations increase:
Saturated fat — 29%
Monounsaturated fat — 50%
Polyunsaturated fat — 21%
How Is Cottonseed Oil Made?
Although cotton farming goes back centuries — with the cultivation of it being evident even in prehistoric times — cottonseed oil production is relegated to more recent history, when it became part of a milling process.25 This is different from mills seen today, which are either screw press or solvent extraction facilities.26 Modern processing of cottonseed oil involves numerous steps, and the main techniques include:27
Because it’s naturally stable, cottonseed oil requires less hydrogenation compared to other oils, and this results in lower trans fat levels.28
Does Cottonseed Oil Have Any Health Benefits?
Some of the health benefits you may have heard about cottonseed oil is that it’s “healthy” because of its high unsaturated fat levels that exhibit total cholesterol-, low-density lipoprotein (LDL)- and triglyceride-lowering properties.29 It’s also touted for producing low levels of trans fats when used for deep-frying foods30 and for its low amounts of saturated fat.31
From a nutrition standpoint, cottonseed oil, along with almond oil and wheat germ oil,32 also has high concentrations of vitamin E,33 a nutrient that may play a role in lowering your risk for diseases, such as Alzheimer’s disease, cardiovascular disease and prostate cancer.
Conventional health experts advise getting vitamin E from vegetable oils like cottonseed oil, because people do not eat foods rich in this nutrient on a daily basis.34,35 It is also believed that vitamin E contributes to the long shelf life of cottonseed oil.36
However, I disagree with these health claims. As much as possible, don’t use vegetable oils like cottonseed oil, whether it’s hydrogenated or not, and whether it’s unrefined or processed. It can negatively impact your health in multiple ways, as explained in the remaining sections. There is only one truly stable and healthful oil to use, and that is high-quality organic coconut oil.
The Drawbacks of Unrefined and Refined Cottonseed Oil
Initially, cottonseed contains gossypol that’s responsible for the oil’s yellowish color.37 This substance can be toxic to nonruminant animals (only adult cattle and sheep are known to metabolize it38) and reacts with protein and lessens the oil’s nutritional value.39
Increased amounts of gossypol have been linked to adverse effects like breathing problems, anorexia and heart, lung, liver and blood cell problems.40 This compound also triggered reproductive health problems among female nonruminant animals, particularly by disturbing “estrous cycles, pregnancy and early embryo development,” and among male animals by causing infertility, sperm immotility and reduced sperm counts.41
In attempts to make this oil less damaging to your health, manufacturers came up with the following areas of improvement for cottonseed oil production:42
Lowering or eliminating gossypol in cottonseed oil
Increasing the yield of cottonseed oil extraction
Increasing the oil’s PUFAs and vitamin E concentrations
Reducing saturated fatty acids
Another step the industry took as far back as 2007 was to implement “educational” marketing campaigns stressing the nutritious aspects of the nonhydrogenated oil, including the fact that “it does not require hydrogenation, the process that produces trans fatty acids,” thus making it “trans fat free.”43,44
And while the U.S. Food and Drug Administration (FDA) banned trans fats and partially hydrogenated oils in May 2018,45,46 the makers of Crisco shortening, a hydrogenated product, was already prepared, having introduced a new trans fat-free version of its product, made from sunflower, soy and cottonseed oils, in 2008.47
Even though being trans fat-free is a good thing, USDA data from July 2018 still show that 94% of the cotton crop grown in American soil is actually genetically engineered, which could leave questions as to how safe or nutritious cottonseed oil really is.48
Although GE proponents dismiss the concerns,49,50GE crops have been linked in the past to possible reproductive problems, organ disruption,51 digestive problems52 and questions about possible allergic reactions.53 Some published reports have also highlighted that cottonseed oil contains a high pesticide load54 and is susceptible to mold contamination.55,56
If You’re Looking for a Healthy Cooking Oil, Here Are the Best Choices
Remember that saturated fat is important for many of your bodily functions, and will not cause heart disease as mainstream recommendations have led you to believe. One of the foods most abundant in saturated and other high-quality healthy fats that is an excellent substitute for cottonseed oil is organic coconut oil.
Coconut oil is ideal for cooking because it’s resistant to high heat damage, and at the same time provides benefits for your overall well being. The article, “Use Coconut Oil Daily” outlines some of the reasons you should make the switch to this oil.
Olive oil is another option you can try, but it must be used cold and drizzled over your favorite foods. It shouldn’t be heated because of its low smoke point, which can cause toxic smoke when used at high heats. For more information on some of the most ideal sources of healthy fats, read “Top 13 Reasons to Replace Dangerous Oils With Healthy Fats.”
It is undeniably the case that both diet and exercise influence the course of aging, though the size of the beneficial effect, even in the case of optimal lifestyle choices, is nowhere near as large as we’d all like it to be. Animal studies show calorie restriction extending maximum life span in mice by up to 40%, as well as lesser effects from various other forms of dietary strategy. Exercise meanwhile doesn’t extend life span in mice, but does postpone age-related dysfunction and disease. Unfortunately, the effects on life span due to any of the strategies that are based on the metabolic effects of exercise and reduced calorie intake scale down as species life span scales up. These lifestyle choices upregulate stress response mechanisms, such as the cellular housekeeping systems of autophagy, resulting in more functional, less damaged cells. Yet calorie restriction, while extending mouse life span significantly, adds no more than a few years at most to human life spans.
That said, the beneficial effects of a good diet and regular moderate exercise are highly reliable, and they cost nothing beyond the time and willpower needed to introduce them into one’s lifestyle. Modest, reliable, and free effects can be worth the effort. Just recognize that, at the end of the day, much more will be needed to avoid the same fate as every other human who has ever lived, aged, and died. We need the development of new biotechnologies capable of addressing the root causes of aging in order to live longer and in better health than can be provided via a good lifestyle. Only technology can purchase us additional decades of healthy life, or extend the human life span by more than a few years beyond its present limits.
The largest study to date of cardiorespiratory fitness in healthy people found that moving more is linked to living longer, regardless of age, sex, and starting fitness level. “People think they have to start going to the gym and exercising hard to get fitter. But it doesn’t have to be that complicated. For most people, just being more active in daily life – taking the stairs, exiting the metro a station early, cycling to work – is enough to benefit health since levels are so low to start with. The more you do, the better.”
The study included 316,137 adults aged 18-74 years who had their first occupational health screening between 1995 and 2015 in Sweden. Cardiorespiratory fitness was measured using a submaximal cycle test and expressed as maximal oxygen uptake (VO2 max) in ml/minute/kg body weight. This is the maximum amount of oxygen the heart and lungs can provide the muscles during exercise. You can estimate your VO2 max using either submaximal cycle tests, treadmill tests, or walking tests. Swedish national registries were used to obtain data on all-cause mortality and first-time cardiovascular events (fatal and non-fatal myocardial infarction, angina pectoris, or ischaemic stroke) during 1995-2015. The risk of all-cause mortality and cardiovascular events fell by 2.8% and 3.2%, respectively, with each millilitre increase in VO2 max.
Power depends on the ability to generate force and velocity, and to coordinate movement. In other words, it is the measure of the work performed per unit time (force times distance); more power is produced when the same amount of work is completed in a shorter period or when more work is performed during the same period. Climbing stairs requires power – the faster you climb, the more power you need. Muscle power gradually decreases after 40 years of age. “We now show that power is strongly related to all-cause mortality. But the good news is that you only need to be above the median for your sex to have the best survival, with no further benefit in becoming even more powerful.”
The study enrolled 3,878 non-athletes aged 41-85 years who underwent a maximal muscle power test using the upright row exercise between 2001 and 2016. The average age of participants was 59 years, 5% were over 80, and 68% were men. During a median 6.5-year follow-up, 247 men (10%) and 75 women (6%) died. Median power values were 2.5 watts/kg for men and 1.4 watts/kg for women. Participants with a maximal muscle power above the median for their sex (i.e. in quartiles three and four) had the best survival. Those in quartiles two and one had, respectively, a 4-5 and 10-13 times higher risk of dying as compared to those above the median in maximal muscle power.
Researchers found that higher diet scores (meaning better diet quality) were strongly associated with decreased odds of physical impairment, including a 25 percent lower likelihood of developing impairment in physical function with aging. An overall healthy diet pattern was more strongly associated with better physical function than an individual component or food. But the team did see that greater intake of vegetables, nuts, and lower intake of red or processed meats and sugar-sweetened beverages each modestly lowered risk of impairment.
It’s possible your penis is shrinking. It’s not right, and it’s not fair. But that’s not the same as not true.
From low testosterone to penile plaque, a variety of things can make your flaccid and/or erect penis smaller.
Although some of them are simply related to age, there are things you can do to mitigate or reverse this loathsome loss of length.
Reverse Penile Atrophy by Boosting Testosterone
Reduced testosterone is the most common cause of penile atrophy. Low testosterone can cause penile atrophy in two different ways:
Testosterone plays a part in the hardness and frequency of your erections. Less testosterone means your erections will appear smaller, and you won’t get hard as frequently.
Very low testosterone can cause a condition called “hypogonadism” , which essentially means the atrophy of your gonads.
If you have low testosterone, many doctors will recommend hormone therapy, which is expensive and can have some nasty side effects.
Luckily, there are plenty of ways to increase your testosterone naturally. Some of my favorites include:
Reduce stress. Stress increases cortisol, which reduces how efficiently your body processes testosterone.
Cut out sugar. Your body produces insulin when you take in sugar, and excess insulin reduces your testosterone levels (source).
Eat testosterone-friendly foods including olive oil, grass-fed beef, butter, cinnamon, broccoli, oysters, onions, garlic and Brazil nuts.
Do “man stuff” like getting outdoors, powerlifting, and competitive sports
(If you think you have low testosterone, read this blog post for more info on how to get it back up).
The more testosterone you produce, the better your penis size and erectile health will be. Most items I just mentioned are easy to implement, so no excuses, gents.
Reverse Penile Atrophy by Reducing Estrogen
Your testosterone levels alone aren’t the only thing you need to be worried about. Your testosterone levels relative to your estrogen levels are just as important.
It’s kind of like your bank account. If you make a lot of money and spend a lot of money, you don’t get ahead nearly as quickly as if you make a lot of money but don’t spend very much.
In this case, upping your testosterone is the making money part. Lowering your estrogen is the spending less part.
Here are some of the easiest ways to “tighten your estrogen belt” so to speak.
Lose your belly fat. Belly fat increases your body’s production of aromatase, which actually converts testosterone into estrogen
Stop drinking beer, instead opt for a glass or two of red wine per week. If you drink beer, avoid hoppy beers.
Cut soy out of your diet completely. Soy is estrogenic, and will cause all sorts of estrogen chaos in your system.
Avoid estrogenic chemicals like BPA, PCB’s and phthalates.
Like with building testosterone, most of these steps aren’t hard to implement (except the skipping the beer one – sorry, guys).
Reverse Penile Atrophy by Using a Penis Pump
Using a penis pump helps fight penile atrophy in two proven ways.
First, it pumps nutrient-rich blood into your penile tissues. This can break up arterial plaque in your penis, restoring healthy blood flow and increasing the size of your erections.
It can even help with severe issues like penile fibrosis or Peyronie’s disease.
Second, penis pumps are proven to increase penis size.
This directly counters the loss of length and girth that happens with penile atrophy.
There are lots of penis pumps out there for you to use. I use and recommend the Bathmate.
Reverse Penile Atrophy by Having More Sex
Turns out the more sex you have, the better you are at sex. Sure, there’s a “practice makes perfect” element here, but more importantly frequent sex makes for better erections.
A recent study in Finland found a a direct relationship between frequency of sex and frequency and quality of erections (source).
This study of over 1,000 men with and without erectile issues demonstrated this was true regardless of other factors.
So, do have sex often…
…but don’t masturbate excessively or use pornography.
Turns out that climaxing with a partner is great for your sexual health. But climaxing too frequently by yourself has the opposite effect.
It confuses your dopamine pathway, which is responsible for sexual arousal, and reduces the frequency and quality of your erections.
Go get laid, gentlemen.
Reverse Penile Atrophy with Herbal Supplements
A variety of herbal supplements have been used to boost fertility and virility for centuries by various populations worldwide.
These herbal remedies boost testosterone, improve blood flow, reduce estrogen, or a combination of all three. There are dozens to choose from, but three stand out as the most effective according to my research and personal experience.
Tongkat ali, which directly improves semen quality, semen quantity, libido, and erectile function (source).
Tongkat also directly improved penis size in men suffering from age-related hypogonadism.
Pine Pollen delivers a solid dose of arginine and superoxide dismutase. Arginine directly improves erectile function, while superoxide dismutase counteracts many of the effects of aging including age-related penile atrophy.
Pine pollen also contains several plant hormones that boost erectile function and sex drive in humans.
Horny Goat Weed, was given its name due to its impact on the sex lives of goats and it does much the same for humans. It improves your levels of nitric oxide (necessary for the physical process of erection), boosts testosterone, and lowers stress hormones that interfere with your sexual health.
Conclusion: How to Reverse Penile Atrophy
The bad news is, penile atrophy isn’t unavoidable. Some of the causes are simply a natural part of aging.
The good news is that many of the causes of atrophy are fairly simple to combat if you remain diligent.
One last thing:QUIT SMOKING. Tobacco use will shrink your gonads. Besides, guys, it’s nasty. If the whole you’ll-die-of-lung-cancer thing isn’t enough, remember: it will shrink your junk.
Disability-adjusted life years (DALYs) are used globally to quantify the number of healthy years of life lost from the presence of a disease, disability, or injury. The burden of chronic, non-fatal health loss and early mortality is evaluated separately and compared across populations. More studies are needed for understanding how aging is linked with disease. Calculating the years lived with a disease (YLDs) and years of life lost (YLLs) from premature mortality will provide insights into the burden of common health conditions for the growing aging adult population. This information can help to identify which health conditions contribute most to the number of healthy years of life lost for aging adults, thereby informing how healthcare providers and interventions prioritize treatment and prevention efforts. The purpose of this study was to determine the burden of 10 common health conditions for a nationally-representative sample of middle-aged and older adults in the United States.
The principal findings of this investigation revealed that over 1-million years of healthy life were lost for middle-aged and older Americans from the 10 health conditions evaluated over the 16 year study period. Although aging adults were impacted by each health condition, hypertension accounted for the greatest burden; whereas, hip fractures had the lowest number of DALYs. There were 30,101 participants included. Sex stratified DALY estimates ranged from 4092 (fractured hip) to 178,055 (hypertension) for men and 13,621 (fractured hip) to 200,794 (hypertension) for women. The weighted overall DALYs were: 17,660 for hip fractures, 62,630 for congestive heart failure, 64,710 for myocardial infarction, 90,337 for COPD, 93,996 for stroke, 142,012 for cancer, 117,534 for diabetes, 186,586 for back pain, 333,420 for arthritis, and 378,849 for hypertension. In total, there were an estimated 1,487,734 years of healthy life lost from the 10 health conditions examined over the study period.
Cholesterol is found in nearly every cell in your body. This waxy substance is vital for optimal functioning of cell membranes, regulating protein pathways and supporting brain health, hormone levels and reducing your heart disease risk. Your body also uses cholesterol to manufacture vitamin D after being exposed to the sun.
As Zoe Harcombe, Ph.D., has noted,1 “It is virtually impossible to explain how vital cholesterol is to the human body. If you had no cholesterol in your body you would be dead.” The majority of the cholesterol in your body, approximately 80%, is manufactured in your liver,2 suggesting your body cannot survive without it.
The remaining 20% is absorbed from the foods you eat but only at a rate of 20 to 60% of what’s in your food. As Alice Lichtenstein, senior scientist and director of the cardiovascular nutrition laboratory at Tufts University, told Eating Well, the absorption rate depends on the individual,3 and if you consume less, your body compensates by making more.
In other words, there is a level at which your body attempts to maintain your cholesterol by manufacturing more or less in response to your dietary intake. Since animals use cholesterol in much the same way as humans, beef, pork and chicken have similar levels of cholesterol in the meat.
In the past decades cholesterol has been vilified as a primary culprit in heart disease. Merck brought the first statin drug, Lovastatin, aka Mevacor, to market in 1987.4,5 Since then, statins have gone on to become the biggest selling class of pharmaceutical compounds of all time, with annual sales in excess of $19 billion in 2017 and projected to reach $24.4 by 2022.6,7 Although the growth has been rapid, recent data demonstrate physicians are not prescribing statins to all eligible patients.8
Physicians Not Offering Statins to Eligible Patients
According to research from the Centers for Disease Control and Prevention (CDC),9 36.7% of U.S. adults over the age of 21 met the eligibility requirements in 2015 for cholesterol lowering treatment with statins as defined by the 2013 guidelines issued by the American College of Cardiology and the American Heart Association.
These guidelines define four groups said to benefit from statins,10 including those with atherosclerotic cardiovascular disease, diabetes and low-density lipoprotein (LDL) cholesterol levels between 70 and 189 milligrams per deciliter (mg/dL). According to the CDC, 55% (43 million American adults)11 who fit the criteria are currently taking statin medication.
Despite these extraordinary numbers, a new study12 from Duke University Medical Center finds 26.5% of U.S. adults who fit the current criteria to use cholesterol-lowering drugs are not taking them. The study is suggesting this occurs since doctors do not offer the drugs to their patients or the patients express concern over the side effects.13
The guidelines were expanded by the U.S. Preventive Services Task Force14 to include individuals who did not have a prior history of heart disease but who had concurrent health conditions that may place them at higher risk for heart attack in the future, such as obesity, high blood pressure, diabetes, high cholesterol and age.
According to the current survey, 59.2%15 who were not taking the drug said their physician had not offered them a prescription. This was most common among women, black people and uninsured patients.
In an email to Reuter’s, Dr. Ian Kronish, associate director of the Center for Behavioral Cardiovascular Health at Columbia University Irving Medical Center, commented on the findings, saying some physicians may not have been completely behind the changes to the guidelines published in 2013, particularly for patients who didn’t have extremely high cholesterol levels or a previous history of heart disease.16
How Do Statins Work?
Statins don’t stop your body from absorbing cholesterol from your food, but rather prevent your liver from making the cholesterol it was designed to produce by blocking an enzyme in the mevalonate pathway called HMG-CoA reductase, used to make cholesterol in the liver.
Essentially, this classification of drugs blocks the mevalonate pathway, which plays a key role in multiple cellular processes, not just the production of cholesterol. Although studied with regard to cholesterol synthesis, the extent of the impact of the mevalonate pathway is not fully understood.17
The drugs also deplete your body of coenzyme Q10 (CoQ10), which may in part account for many of its devastating long-term results. A black box warning was proposed to warn patient and physicians about this reduction in CoQ10,18 but in 2014 the FDA decided against it.19
CoQ10 is used in energy production by every cell in your body and is vital for optimal health and longevity. In its reduced form, ubiquinol, it’s a crucial component of cellular respiration and the production of adenosine triphosphate (ATP), a coenzyme used as an energy carrier in every cell in your body. Since your heart is the most energy demanding organ, depleting this energy supply can have devastating consequences.
Former FDA Commissioner Had Strong Ties to Big Pharma
The featured study was performed at Duke University by scientists with a history of producing research supporting statin use and calling for a greater number of prescriptions in patients who may not have had a previous history of heart disease,20,21,22,23,24 continuing a legacy of pharmaceutical support left by Dr. Robert Califf,25 who served as U.S. Food and Drug Administration (FDA) commissioner from February 2016 until January 2017.26
In May 2014, Califf, a Duke cardiologist and study chairman, gave a presentation27 to a group of experts, describing ways to increase the pace of innovation through the transformation of the research process. Specifically, his last slide called for a plan to simplify the regulatory systems governing research, believing it may have slowed biomedical innovation.
This was near the end of his association with Duke University, as he was soon to be nominated by then President Barack Obama as the FDA commissioner.28 During his confirmation hearings he defended his position in accepting drug industry funding and promised to not lower the agency’s safety standards.
When questioned by senators, Califf attempted to disarm his previous statement that regulations governing research were too complicated and slowed innovation by saying,29 “I’ve never been a proponent of lowering standards. If anything, I’ve argued for raising them.”
According to The New York Times,30 Califf had been associated with scientific papers produced by pharmaceutical company researchers, he’d been paid by seven drug companies and a device maker for consulting services, and his university salary was partially supported by drug companies, including Merck, Novartis and Eli Lilly.
In a conflict of interest section at the end of one paper, he declared financial support from more than 20 companies and research entitites.31 Daniel Carpenter, a Harvard political science professor with an expertise in the FDA calls him the “ultimate industry insider.”32
Califf also resigned from the board of directors at Portola Pharmaceuticals on January 26, 2015, just prior to his nomination as FDA commissioner, having received compensation of $259,623.33
Recently, Duke Clinical Research Institute paid $112.5 million to settle claims that bogus research data34 were submitted to the National Institutes of Health to acquire grant money for research.35 Seven years of data were determined to be unreliable.
Risks Associated With Statins Supported by Science
Among those who were offered but declined statins in the featured study,36 the most common reason stated was fear of side effects from the drugs.37 Senior study author Dr. Ann Marie Navar from the Duke Clinical Research Institute38 believes public perception of side effects is unrealistic. She commented:
“Although there are risks associated with statins, the public fear of side effects is out of proportion to the actual risks. Misconceptions about statins are everywhere and are fueled by false information on the internet.”
However, despite Navar’s attempt to downplay the side effects of statin medications, the risks are well-documented and supported by scientific evidence, so the fears are well-founded. According to the FDA:39
There have been rare reports of serious liver problems. Patients should notify their health care professional right away if they have the following symptoms: feeling unusually tired or weak; loss of appetite; upper belly pain; dark colored urine; yellowing of the skin or the whites of the eyes.
Memory loss and confusion have been reported. The conditions are generally non-serious and reversible after stopping statin use.
Increases in blood sugar levels have been reported.
Before starting a statin, patients should inform their health care professional about all medicines that they are taking or plan to take. Some medicines may interact with statins, increasing the risk for side effects.
However, these are only the side effects acknowledged by the FDA and not the full scope of the effects supported by research. A reduction in CoQ10 triggered by this classification of drugs may increase your risk of acute heart failure40 and atherosclerosis, as found in data published in Expert Review of Clinical Pharmacology.41
The study addressed several physiological mechanisms, including how the drug inhibits the synthesis of vitamin K2, which is responsible for protecting your arteries from calcification. One of its biological roles is to move calcium out of your blood and into the proper areas of your body, such as your bones and teeth.
Since statins inhibit the function of vitamin K2,42 it may place you at risk of deficiency, which may contribute to osteoporosis, heart disease, brain disease and inappropriate calcification. The same enzyme used by your liver to produce cholesterol that is inhibited by statins is also involved in the production of ketone bodies.
The depletion of CoQ10 and the inhibition of vitamin K2 also increases your risk of other serious diseases including cancer. Long-term statin use more than doubles a woman’s risk of two types of breast cancer,43 and significantly increases a man’s risk for prostate cancer.44 Research has also associated statin use with an increased risk of diabetes,45,46,47 neurodegenerative diseases,48 cataracts49,50 and musculoskeletal disorders.51
How to Evaluate Your Risk of Heart Attack
As you consider whether taking statins make sense for your health, it’s important to understand what your cholesterol numbers mean. Your total cholesterol is not a strong indicator of your risk of heart disease. Better indicators are:
The ratio of your high-density lipoprotein (HDL) to total cholesterol — To get this number, divide your HDL level by your total cholesterol and multiply by 100 to get the answer. Ideally, your HDL to cholesterol ratio would be 24% or above.
Your triglyceride to HDL ratio — Your triglyceride to HDL ratio should ideally be below 2.
Two tests that are even more important for assessing your cardiovascular disease risk are your serum ferritin and gamma glutamyl transpeptidase (GGT). The GGT is used as a screening marker for excess free iron and a great indicator of your risk of sudden cardiac death. The recommended and ideal levels of ferritin and GGT are as follows. For more information about these tests, read my previous article, “Cholesterol Does Not Cause Heart Disease.”
• Ferritin — Adult men and non-menstruating women: 30 to 40 nanograms per milliliter (ng/mL) or 75 to 100 nanomoles per liter (nmol/L).
The most commonly used threshold for iron deficiency in clinical studies is 12 to 15 ng/mL (30 to 37 nmol/L). You do not want to be below 20 ng/mL (50 nmol/L) or above 80 ng/mL (200 nmol/L). High iron during pregnancy is also problematic; having a level of 60 or 70 ng/mL (150 or 175 nmol/L) is associated with greater odds of poor pregnancy outcomes.
• GGT — Below 16 units per liter (U/L) for men and below 9 U/L for women. Above 25 U/L for men and 18 U/L for women, your risk of chronic disease increases significantly.
Protect Your Heart and Lower Your Risk of Heart Disease
Avoid environmental pollutants and toxins, including smoking, vaping, heavy metals, herbicides and pesticides, especially glyphosate.
Minimize your exposure to electromagnetic fields and wireless radiation from cellphones, Wi-Fi, routers, smart meters and more, as this kind of radiation has been shown to cause serious free radical damage and mitochondrial dysfunction.
Eat an unprocessed whole food-based diet low in net carbs and high in healthy fats. A ketogenic diet — which is very low in net carbohydrates and high in healthy fats — is key for boosting mitochondrial function.
When your body is able to burn fat for fuel, your liver creates water-soluble fats called ketones that burn more efficiently than carbs, thereby creating fewer reactive oxygen species and secondary free radicals. Ketones also decrease inflammation and improve glucose metabolism.52
Eat nitrate-rich foods to help normalize your blood pressure. Good sources include arugula, cilantro, rhubarb, butter leaf lettuce, mesclun mixed greens, beet greens, fresh beet juice, kvass (fermented beet juice) and fermented beet powder.
Get plenty of nonexercise movement each day; walk more and incorporate higher intensity exercise as your health allows.
Intermittently fast. After you’ve become accustomed to intermittently fasting for 16 to 18 hours, you may try a stricter fast once or twice a week, when you eat a 300- to 800-calorie meal loaded with detox supporting nutrients, followed by a 24-hour fast. So, in essence, you’re then only eating one 300- to 800-calorie meal in 42 hours.
If you have heart disease, consider enhanced external counterpulsation (EECP). To find a provider, see EECP.com.53
If you have heart disease, you may also consider taking g-strophanthin, an adrenal hormone helping to create more parasympathetic nervous system neurotransmitters, thereby supporting your parasympathetic nervous system. It also helps flush out lactic acid. Strophanthus is the name of the plant, the active ingredient of which is called g-strophanthin in Europe, and ouabain in the U.S.
Get sensible sun exposure to optimize your vitamin D status and/or take an oral vitamin D3 supplement with magnesium and vitamin K2.
Implement heart-based wellness practices such as connecting with loved ones and practicing gratitude.