healthy body weight Archives - Amazing Health Advances

An Ideal BMI

The AHA! Team — Fri, 18 Jul 2025 05:15:35 +0000

Michael Greger M.D. FACLM via Nutrition Facts – Is there a unisex chart for optimal weight based on height? We seem to have become inured to the mortal threat of obesity. If you go back in the medical literature almost a quarter of a century ago when obesity wasn’t run-of-the-mill, the descriptions are much grimmer: “Obesity is always tragic, and its hazards are terrifying.” Not just obesity, though. Of the four million deaths attributed to excess body fat each year, nearly 40 percent of the victims are overweight, not obese. According to two famous Harvard studies, weight gain of as little as 11 pounds (5 kg) from early adulthood through middle age increases the risk of major chronic diseases, such as diabetes, cardiovascular disease, and cancer. The flip side, though, is that even modest weight loss can have major health benefits. What is the optimal body mass index, commonly known as BMI? The largest studies in the United States and around the world found that having a BMI of 20 to 25 is associated with the longest lifespan. Put all the best available studies with the longest follow-up together, and that can be narrowed down even further to a BMI of 20 to 22. That would be about 124 to 136 pounds (56 to 62 kg) for someone who’s five-foot-six (168 cm), as you can see below and at 1:22 in my video What’s the Ideal BMI?. Even within a “normal” BMI range, the risk of developing chronic diseases, such as type 2 diabetes, heart disease, and several types of cancer, starts to rise towards the upper end—starting as low as a BMI of 21. BMIs of 18.5 and 24.5 are both considered to be within the “normal” range, but a BMI of 24.5 may be associated with twice the risk of heart disease compared to a BMI of 18.5. Below and at 2:05 in my video is a graph of diabetes risk and BMI among women. There is a fivefold difference in diabetes rates within the so-called ideal range with a BMI under 25. Just as there are gradations of risk within a normal BMI range, there is a spectrum within obesity. Class III obesity (BMI over 40) can be associated with the loss of a decade or more of life. At a BMI above 45, for example, a person standing at 5’6″ (168 cm) and weighing 280 pounds (127 kg), life expectancy may shrink to that of a cigarette smoker. Skeptics have argued However, “skeptics have argued that the consequences of rising obesity levels have either been greatly exaggerated or are unclear.” A “motley crew,” “obesity skeptics are made up of a kaleidoscope of interest groups…includ[ing] feminists, queer theorists, libertarians, far right-wing conspiracy types and new ageists.” It “has also been popular on far right-wing, pro-gun, pro-America websites where the idea that obesity alarmists are nanny-state communists who simply want to stop us from having fun plays well….” Less treatment of the problem Unlike activists who organized to raise consciousness and stamp out the AIDS epidemic, for example, some in the size acceptance movement appear to have the opposite goal and “have called for less public awareness and intervention regarding obesity,” less treatment of the problem. I’m all for fighting size stigma and discrimination—I have a whole section on weight stigma in my book How Not to Diet—but the adverse health consequences of obesity are an established scientific fact. Can’t you be fat but fit? In a study of more than 600 centenarians, only about 1 percent of the women and not a single one of the men were obese. There does appear to be a rare subgroup of individuals who are obese and do not suffer the typical metabolic costs, such as high blood pressure and cholesterol. This raises the possibility that there may be such a thing as “benign obesity” or “metabolically healthy obesity.” It may just be a matter of time, though, before the risk factors develop. Even if they don’t, though, when followed long enough, even “metabolically healthy obese adults” are at increased risk of diabetes, as well as increased risk of fatty liver disease. They are also at greater risk of cardiovascular events, such as heart attacks, and/or premature death, as shown below and at 4:20. Bottom line? There is “strong evidence that ‘healthy obesity’ is a myth.” Many “fat activists” try to downplay the risks of obesity, even as they may be among “the greatest victims” of the epidemic. “Leading fat acceptance activist Lynn McAfee, who is director of medical advocacy for the Council on Size and Weight Discrimination and takes part in obesity conferences and government panels on obesity,” is quoted as saying, “‘I’m not actually particularly that interested in [health] and God I hate science….” If you missed the previous blog posts in this series on obesity, see related posts below. The final video in this series is What’s the Ideal Waist Size?. Key Takeaways Nearly 40 percent of the four million deaths linked to excess body fat annually are among people who are overweight, not just obese, showing the widespread health risks. Even small reductions in body weight can significantly improve health outcomes, reducing the risk of chronic diseases like diabetes, heart disease, and cancer. The optimal BMI for longevity is between 20 and 22, with risks for diseases increasing even within the “normal” BMI range, especially towards the upper end. Some groups, including far-right and size acceptance activists, downplay or deny the health risks of obesity, despite overwhelming scientific evidence linking it to serious health issues. Although some individuals may appear metabolically healthy while obese, long-term studies show that they still face heightened risks of conditions like diabetes, fatty liver disease, and heart attacks, debunking the idea of “healthy obesity.” To read the original article click here.

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Epigenetics and Obesity

The AHA! Team — Tue, 03 Dec 2024 06:06:42 +0000

Michael Greger M.D. FACLM via Nutrition Facts – Identical twins don’t just share DNA; they also share a uterus. Identical twins don’t just share DNA; they also share a uterus. Might that help account for some of their metabolic similarities? “Fetal overnutrition, evidenced by large infant birth weight for gestational age, is a strong predictor of obesity in childhood and later life.” Could it be that you are what your mom ate? A dramatic illustration from the animal world is the crossbreeding of Shetland ponies with massive draft horses. Either way, the offspring are half pony/half horse, but when carried in the pony uterus, they come out much smaller, as you can see below and at 0:47 in my video The Role of Epigenetics in the Obesity Epidemic. (Thank heavens for the pony mother!) This is presumably the same reason why the mule (horse mom and donkey dad) is larger than the hinny (donkey mom and horse dad). The way you test this in people is to study the size of babies from surrogates after in vitro fertilization. Who do you think most determines the birth weight of a test-tube baby? Is it the donor mom who provided all the DNA or the surrogate who provided the intrauterine environment? When it was put to the test, the womb won. Incredibly, a baby who had a thin biological mother but was born to a surrogate with obesity may harbor a greater risk of becoming obese than a baby with a heavier biological mother but born to a slim surrogate. The researchers “concluded that the environment provided by the human mother is more important than her genetic contribution to birth weight.” The most compelling data come from comparing obesity rates in siblings born to the same mother, before and after her bariatric surgery. Compared to their brothers and sisters born before the surgery, those born when mom weighed about 100 pounds less had lower rates of inflammation, metabolic derangements, and, most critically, three times less risk of developing severe obesity—35 percent of those born before the weight loss were affected, compared to 11 percent born after. The researchers concluded that “these data emphasize how critical it is to prevent obesity and treat it effectively to prevent further transmission to future generations.” Hold on. Mom had the same DNA before and after surgery. She passed down the same genes. How could her weight during pregnancy affect the weight destiny of her children any differently? Darwin himself admitted, “In my opinion, the greatest error which I have committed, has been not allowing sufﬁcient weight to the direct action of the environment, i.e. food…independently of natural selection.” We finally figured out the mechanism by which this can happen—epigenetics. Epigenetics, which means “above genetics,” layers an extra level of information on top of the DNA sequence that can be affected by our surroundings, as well as potentially passed on to our children. This is thought to explain the “developmental programming” that can occur in the womb, depending on the weight of the mother—or even the grandmother. Since all the eggs in your infant daughter’s ovaries are already preformed before birth, a mother’s weight status during pregnancy could potentially affect the obesity risk of her grandchildren, too. Either way, you can imagine how this could result in an intergenerational vicious cycle where obesity begets obesity. Is there anything we can do about it? Well, breastfed infants may be at lower risk for later obesity, though the benefits may be confined to those who are exclusively breastfed, as the effect may be due to growth factors triggered by exposure to the excess protein in baby formula, as you can see below and at 3:51 in my video. The breastfeeding data are controversial, though, with charges leveled of a “white hat bias.” That’s the concern that public health researchers might disproportionally shelve research results that don’t fit some goal for the greater good. (In this case, preferably publishing breastfeeding studies showing more positive results.) But, of course, that criticism came from someone who works for an infant formula company. Breast is best, regardless. However, its role in the childhood obesity epidemic remains arguably uncertain. Prevention may be the key. Given the epigenetic influence of maternal weight during pregnancy, a symposium of experts on pediatric nutrition concluded that “planning of pregnancy, including prior optimization of maternal weight and metabolic condition, offers a safe means to initiate the prevention rather than treatment of pediatric obesity.” Easier said than done, but overweight moms-to-be may take comfort in the fact that after the weight loss in the surgery study, even the moms who gave birth to kids with three times lower risk were still, on average, obese themselves, suggesting weight loss before pregnancy is not an all-or-nothing proposition. What triggered the whole obesity epidemic to begin with? There are a multitude of factors, and I covered many of them in my 11-video series on the epidemic in the related posts below. We are what our moms ate in other ways, too. Check out: Heart Disease May Start in the Womb Maternal Diet May Affect Stress Responses in Children Flashback Friday: The Effect of Animal Protein on Stress Hormones, Testosterone, and Pregnancy Key Takeaways Babies who are born larger are at higher risk of obesity later in life, suggesting early metabolic programming by maternal diet. The intrauterine environment significantly influences birth weight and later obesity risk, potentially outweighing genetic contributions from the biological mother. A baby with a thin biological mother but born to a surrogate with obesity may harbor a greater risk of future obesity than a baby with a heavier biological mother but born to a slim surrogate. Siblings born to the same mother before and after her bariatric surgery show reduced obesity risk in later-born children, highlighting the critical role of maternal weight during pregnancy. Epigenetics explain how environmental factors, like maternal weight, can influence gene expression and obesity risk across generations. Breastfeeding, especially exclusive breastfeeding, may lower obesity risk in children, contrasting with potential risks associated with formula feeding and excess protein exposure. To read the original article click here.

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The Bizarre Link Between Oreos and Hot Flashes

The AHA! Team — Mon, 04 Nov 2024 06:05:32 +0000

Al Sears, MD, CNS – If you’ve ever eaten an Oreo, you’ve probably noticed how hard it was to eat just one. Don’t worry, it’s not just you! Research has found that Oreos are more addictive than cocaine.[1] A big reason for that is the fact that the cookies are loaded with the artificial sweetener high-fructose corn syrup (HFCS). A Canadian study found that HFCS can cause behavioral reactions similar to those produced by common street drugs.[2] Other research shows that HFCS and cocaine stimulate the same brain circuits. I know what you’re probably thinking… What does all this have to do with hot flashes? Let me explain. As you probably know, HFCS is in a lot of foods that make up the standard American diet. It’s a big part of the reason we have an obesity epidemic in our country. But HFCS does more than make you gain weight. It also causes fat to build up in your liver. When that happens, you can end up with a condition called fatty liver disease. Over the last 10 to 15 years, I’ve seen a sharp increase in the number of patients with fatty liver disease at my clinic – in both men and women. But for women, the symptoms of fatty liver disease can look a lot like menopause. Symptoms like night sweats, exhaustion, extra weight around the abdomen… and hot flashes. That’s why so many mainstream doctors miss this diagnosis. They write the symptoms off as “women’s problems.” The truth is, you could have fatty liver disease and not even know it. Liver diseases are one of the fastest-growing health epidemics in the world. According to a new study, today up to 50% of Americans suffer from nonalcoholic liver disease (NAFLD) – including children as young as 2 years old.[3] And HFCS is a big contributor. You see, HFCS isn’t like other sugars. Most of it goes straight to your liver instead of going into your muscles and tissues for energy. It promotes the formation of new fat molecules. It triggers your liver cells to store this fat where it doesn’t belong. At the same time, it blocks the breakdown of old fats. A study from the University of Florida found patients with fatty liver disease ate two to three times more high fructose corn syrup.[4] And just like alcohol, this cheap fructose is addictive. Once you start eating it, you crave even more sweets. Corn syrup floods your bloodstream, overwhelming your liver’s processing capacity. Your liver becomes inflamed and develops into NAFLD. 3 Simple Tips to Improve Your Liver Health Mainstream medicine has no treatments for this condition. However, I help my patients treat fatty liver disease with three simple, natural solutions. Supplement with DHA. Researchers found that supplementing with the omega-3 fatty acid DHA stops fatty liver disease in its tracks. In the study, they fed animals a Western-style diet that leads to obesity. Then they gave them DHA. The team found that DHA blocked the progression of the worst form of fatty liver disease – even though the animals continued to eat the same dangerous diet.[5] In a human study, volunteers taking 1,000 mg per day of omega-3s decreased serum markers of liver cell damage and levels of triglyceride fats.[6] You see, DHA is anti-inflammatory. It helps to heal liver cell membranes. DHA also suppresses the production of new liver fat cells and stimulates the burning of fat cells. You can get DHA from grass-fed meats and organs. But it’s almost impossible to get enough from your diet. I advise my patients to supplement with between 600 mg and 1,000 of DHA daily from a combination of squid oil and krill oil. Take the liver herb. Milk thistle is also known as the “liver herb.” It has an active compound called silymarin. In a placebo-controlled study of 100 patients, silymarin promoted a significant decline in liver enzyme markers. That indicated a reversal of NAFLD with no serious side effects.[7] Use my favorite supplement. A study in the Journal of the American College of Nutrition proved that CoQ10 can also treat NAFLD.[8] The trial included 41 people with mild to moderate NAFLD. Researchers gave half the patients 100 mg of CoQ10 every day. The other half got a placebo. After 12 weeks, all signs of NAFLD were lower in the CoQ10 group. Four of the patients on CoQ10 even returned to normal liver function. You can get CoQ10 from grass-fed organ meat and beef, game, and wild-caught fatty fish. But again, it’s hard to get all you need from diet alone. Normally, I recommend 50 mg daily. But to treat NAFLD, I suggest taking 100 to 300 mg per day of the ubiquinol form of CoQ10. Divide it into two doses. References [1] Connecticut College News, October 15, 2013 [2] Addiction to unhealthy foods could help explain the global obesity epidemic. EurekAlert! [3] Cha A. “Fatty liver disease was a disease of the old. Then kids started getting sick.” https://www.washingtonpost.com/health/interactive/2023/nonalcoholic-fatty-liver-disease-kids/. [4] Lyssoiotis C, Cantley. “F stands for fructose and fat.” Nature. 2013;502:181-182. [5] https://synergies.oregonstate.edu/2017/dha-offers-hope-to-stop-deadly-march-toward-cirrhosis-liver-cancer/ [6] Capanni M, et al. “Prolonged n-3 polyunsaturated fatty acid supplementation ameliorates hepatic steatosis in patients with nonalcoholic fatty liver disease: a pilot study.” Aliment Pharmacol Ther. 2006 Apr 15;23(8):1143-51. [7] Hashemi et al. “A placebo-controlled trial of silymarin in patients with nonalcoholic fatty liver disease.” Hepatitis Monthly. 2011;9(4):265-270. [8] Farnaz Farsi et al. “Functions of Coenzyme Q10 Supplementation on liver enzymes, markers of systemic inflammation, and adipokines in patients affected by nonalcoholic fatty liver disease: A double-blind, placebo-controlled, randomized clinical trial.” J Am Coll Nutr. 2016;35(4):346-353 To read the original article click here.

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Does Marijuana Affect Weight Gain or Bone Density?

The AHA! Team — Wed, 23 Oct 2024 08:19:02 +0000

Michael Greger M.D. FACLM via Nutrition Facts – Are the apparent adverse effects of heavy cannabis use on the bone just due to users being thinner? It’s been recognized for decades that cigarette smoking can have “a major effect” on bone health, “increasing the lifetime risk of hip fracture by about half.” It also appears to impair bone healing, so much so that surgeons ask if they should discriminate against smokers because their bone and wound-healing complication rates are so high. What about smoking marijuana? As I discuss in my video Effects of Marijuana on Weight Gain and Bone Density, “There is accumulating evidence to suggest that cannabinoids [cannabis compounds] and their receptors play important roles in bone metabolism by regulating bone mass, bone loss, and bone cell function.” Okay, but are they “friend or foe?” “Results from research on cannabinoids and bone mineral density in rodent models have been inconsistent. Some studies show increased bone formation, others have demonstrated accelerated bone loss, and yet others have shown no association. This variation in results may be due [in part] to differences in the mouse strain, sex, age…” If you can’t even extrapolate from one mouse to another, how can you extrapolate from mice to human beings? What if you just measure cannabis use and bone mineral density in people? Researchers tested thousands of adults and asked them about their cannabis use. There did not appear to be any link between the two, which is a relief. However, in this study, “heavy” cannabis use was defined as just five or more days of use in the previous 30 days. The researchers didn’t ask beyond that, so, theoretically, someone who smoked just five joints in their entire life could be categorized as a “heavy user” if they happened to use it five times in the last four weeks. How about cannabis use on 5,000 separate occasions over a lifetime? Now that’s a heavy user—decades of regular use. In that case, heavy use was “associated with low bone mineral density and an increased risk of fractures”—about double the fracture rate presumably due to lower bone density in the hip and spine, although heavy cannabis users were also thinner on average, and thinner people have lighter bones. Hip fracture risk goes down as our weight goes up. Nearly half of underweight women have osteoporosis, but less than 1 percent of obese women do, which makes total sense. Being obese forces our body to make our bones stronger to carry around all of that extra weight. That’s why weight-bearing exercise is so important to constantly put stress on our skeleton. When it comes to our bones, it’s use it or lose it. That’s why astronauts can lose a percent of their bone mass every month in “long-duration spaceflight.” Their bodies aren’t stupid. Why waste all that energy making a strong skeleton if you aren’t going to put any weight on it? So, maybe the reason heavy cannabis users have frailer bones is because they tend to be about 15 pounds lighter. Wait a second. Marijuana users are slimmer? What about the munchies? “The lower BMI that was observed in heavy cannabis users at first sight seems counterintuitive,” given marijuana’s appetite stimulation, but this isn’t the first time this has been noted. “Popular culture commonly depicts marijuana users as a sluggish, lethargic, and unproductive subculture of compulsive snackers,” and marijuana has indeed been found to increase food intake. A single hit can increase appetite, so you’d expect obesity rates to rise in states that legalized it. But, if anything, the rise in obesity appeared to slow after medical marijuana laws were passed, whereas it appeared to just keep rising in other states, as you can see in the graph below and at 3:45 in my video. The reason pot smokers may be slimmer is because of the effect of smoked marijuana on metabolism. We’ve known for more than nearly 40 years that within 15 minutes of lighting up, our metabolic rate goes up by about 25 percent and stays there for at least an hour, as you can see below and at 4:04 in my video. So, that may be playing a role. Is that why heavy cannabis use is associated with lower bone mineral density and increased risk of fractures? Because users just aren’t as overweight? No. Even when taking BMI into account, heavy cannabis use appears to be “an independent predictor” of weaker bones. I originally released a series of marijuana videos in a webinar and downloadable digital DVD. There are still a few videos coming out over the next year, but if you missed any of the already published ones, see the related posts below. For more on bone health, check out the related posts below. Key Takeaways Cigarette smoking is known to have a major negative effect on bone health, increasing the risk of hip fracture and impairing bone healing. Surgeons questioned whether they should discriminate against smokers due to higher complication rates. Cannabinoids and their receptors are implicated in bone metabolism, influencing bone mass, bone loss, and bone cell function. However, research on cannabinoids’ effects on bone mineral density in rodents has shown inconsistent results. Heavy cannabis use, defined as more than 5,000 separate occasions over a lifetime, is “associated with low bone mineral density and an increased risk of fractures.” This risk is about double compared to non-heavy users, potentially due to users’ lower bone density in the hip and spine. Heavy cannabis users, despite experiencing increased appetite (the munchies), tend to have lower BMI and are slimmer. The increased metabolic rate observed after smoking marijuana may contribute to this, but heavy cannabis use remains an independent predictor of weaker bones, even when considering BMI. To read the original article click here.

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10 Shocking Facts About Cholesterol You Don’t Know

The AHA! Team — Mon, 27 May 2024 08:05:28 +0000

Dr. Don Colbert – Do you really know what you need to know about cholesterol? Do you know the truth about how diet does and does not affect it? How about how body weight affects it? Do you really know what you need to know about cholesterol? Surprisingly, even though cholesterol has been discussed for many decades, the facts about cholesterol are still lost on most. Why? Misinformation abounds. New studies shed new light on the subject. As our population has become increasingly overweight, people’s bodies (all the way down to their cells) change in how they synthesize and deal with cholesterol. To know the facts about cholesterol, you really have to dig in. It’s simple and yet complex in some ways. If you’re ready for the complete low-down on cholesterol, listen to the Divine Health Podcast! Dr. Colbert and Mary Colbert will take you on an in-depth journey to know all you need to know about cholesterol and how to obtain your best heart health! Check out all 3 cholesterol episodes here: Divine Health with Dr. Don Colbert Podcast. And for now, here are 10 shocking facts about cholesterol you probably don’t know. 10 Shocking Facts About Cholesterol You Don’t Know A heart healthy diet is imperative for overall heart health. But when it comes to cholesterol itself in the bloodstream, most is made by the body, not consumed in the diet. In fact, only about 20% of the cholesterol in your body comes from your diet. The rest is synthesized in your liver and intestines (1). How does diet play a role? Many ways! First, your diet affects how much, and what types of cholesterol are synthesized. In fact, the types of fats you eat play a bigger role than the cholesterol you eat. Next, eating a diet high in antioxidants is paramount, since antioxidants reduce the amount of oxidized cholesterol (which forms plaques) in the arteries. Vegetable oils do not contain cholesterol, however, many are still inflammatory and detrimental to heart health. Oils derived from vegetables and grains, including avocado oil, olive oil, corn oil, and others have zero milligrams of cholesterol. Foods derived from plants do not contain cholesterol because cholesterol is synthesized in an animal’s liver. However, vegetable oils with high omega-6 content increase inflammatory pathways in our bodies because they negatively affect our ratio of omega-3s to omega-6s. This means they fight against the anti-inflammatory omega-6s in our bodies. The most commonly used high-omega-6 oil in processed foods is soybean oil. Consuming this oil negatively affects metabolic health, cardiovascular health, and inflammation in the body (2, 3, 4). Avoid: Safflower oil (10.1 gm Omega-6 per tablespoon), grapeseed oil (9.5 gm), vegetable Oil (7.9 gm), wheat germ oil (7.5 gm), corn oil (7.3 gm), walnut oil (7.3 gm), cottonseed oil (7.0 gm), soybean (7.0 gm), sunflower Oil (5.4 gm), canola Oil (3.0 gm). Include: Extra-virgin olive oil (1.3 gm), avocado oil (1.8 gm) and occasionally organic coconut oil (0.4 gm), high-oleic sunflower (0.5), and high-oleic safflower oils (2.0). To learn more about this ratio and the dangers of a high omega-6 diet, click here. Weight Loss, Diet, and Exercise are your best options to ALTER unhealthy cholesterol numbers. While your absolute cholesterol number is highly influenced by your familial history, age, sex, and ethnicity (5), CHANGES in total cholesterol are primarily achieved by weight loss (if overweight), diet, and exercise (6, 7). Your Body Needs Cholesterol for Crucial Tasks Such as Synthesizing Vitamin D. Cholesterol is a waxy, whitish-yellow fat. Cholesterol is needed to make vitamin D, hormones (including testosterone and estrogen), and fat-dissolving bile acids. It is a vital building block in cell membranes. Cholesterol can be found in every cell in the body. What’s more, cholesterol is important for the formation of myelin sheath, the protective membrane around the nerves, especially in early years of life. Healthy cholesterol has its place in human health. Cholesterol does NOT dissolve in the blood to make it thick. Cholesterol doesn’t dissolve in the blood, kind of like how fat won’t dissolve in water. Instead, cholesterol bonds to carriers called lipoproteins. Lipoproteins are made up of cholesterol on the inside with a layer of protein on the outside. These carriers transport cholesterol between cells to be used for various biological functions. When cholesterol is oxidized, it can embed into the artery wall which can lead to plaques and blockages. Not all LDL cholesterol (aka bad cholesterol) creates plaques in arteries. As most people know, there are two primary types of cholesterol, Low-density lipoproteins (LDL) and High-density lipoproteins (HDL) cholesterol. LDL cholesterol is taught as “bad,” and HDL as “good.” But there’s more to it than that. There are actually two sub-groups of LDL particles. LDL subtype A is a large fluffy cholesterol particle that is less prone to oxidation and less likely to stick to arterial walls. LDL subtype B is a smaller and denser particle that is easily oxidized and more likely to build up in the arteries. Subtype A LDL cholesterol is not necessarily a threat, and only oxidized LDL cholesterol forms plaques (8). Triglyceride numbers and cholesterol numbers should be looked at together when assessing cardiovascular risk. Interestingly, more and more practitioners are looking at the ratio of triglycerides (TG) to HDL. In fact, when you calculate this ratio, you can infer your health risk of cardiovascular issues, blood sugar issues, inflammation and more. Divide your triglycerides by your HDL cholesterol levels. Studies have found that a number of 1.0 or less is likely indicative of lower risk, and a number of 3.0 or more of highest risk. Interestingly, a lower ratio is also linked to healthier LDL subset particle size (less subset B) (9, 10). People who suffer heart attacks don’t always have high cholesterol. Conversely, those with high cholesterol don’t always suffer heart attacks. While high LDL cholesterol (specifically, high LDL subset B) is one of many risk factors of heart conditions and heart attacks, many people who have heart attacks have “normal” cholesterol levels (11). When assessing risk, we should look at our heart illness risk overall, including weight, blood glucose, lifestyle, inflammation markers, blood pressure, triglycerides, and specifically LDL Subset B cholesterol numbers. It is not the primary risk factor. Inflammation is a primary factor in cardiovascular risk. Cholesterol is an active compound in the body. It reacts to oxidative stress and inflammation. Here’s how: As free radicals move throughout the body and damage cells, cumulative oxidative stress rises. Next, the body mounts an inflammatory response and cholesterol comes in to patch things up. When cholesterol can also become damaged and oxidized by free radicals. Oxidized cholesterol is sticky. It can embed into artery walls and potentially form plaques and blockages (12). Statins may be useful in some, but they are not completely safe and effective. While statins may be right for some patients, no medication is completely safe, and no medication is completely effective. While it is true that statins typically lower overall cholesterol, there are some harmful side effects of which you should be aware. First, statins may lower total cholesterol too much. This can lead to inadequate cholesterol levels for proper brain function (25% of cholesterol is in the brain). It can also interfere with and inhibit the benefits of omega-3 fats. Statins metabolize omega-6 fatty acids which work against omega-3s and can promote resistance to insulin, and elevated blood glucose levels. Like most medications, statins include a risk of damage to organs and systems in the body (13). Lastly, chronic use of statins has also been shown to interfere with the body’s production of coenzyme Q10 (CoQ10). CoQ10 is critical for immune and nervous system health, and also bolsters heart health, proper muscle function, and healthy blood pressure, among much else. If you are on statins, it is very important to supplement with CoQ10. Ready to Do All You Can to Support Healthy Cholesterol Numbers and Heart Health? Dr. Colbert has devised an amazing guide to help you obtain a healthy weight, healthy cholesterol, and overall great health for life: Beyond Keto. When you follow this plan that marries the best of the Mediterranean Diet with the best of Keto Zone, you can optimize your health efficiently and effectively. Try Beyond Keto and get started today. Then, listen to the podcast and learn even more facts about cholesterol! Bottom Line After decades of confusing information, new studies, changes in lifestyles and societal health, and more, it’s important to learn the facts about cholesterol. Learn all you can. Listen to Dr. Colbert’s Podcast, it’s a wealth of free information to keep you up to date on what you can do to support your heart health and cholesterol numbers, every day. To read the original article click here.

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Natural Compound Boosts Serotonin Levels, Supports Healthy Weight, New Study Suggests

AHA Publisher — Mon, 24 Oct 2022 07:00:48 +0000

Lori Alton via NaturalHealth365 – According to the Centers for Disease Control, a shocking 73 percent of American adults are currently either overweight or obese – setting the stage for soaring rates of type 2 diabetes and nonalcoholic fatty liver disease. In addition, experts report that the incidence of major depression – with symptoms of fatigue, anxiety, and insomnia – is on the rise in the United States as well. What could be behind this epidemic of less-than-optimal physical and psychological health? Many researchers believe that low levels of serotonin – a neurotransmitter needed for normal appetite, restful sleep, and stable mood – can play a role. Recent studies highlight the potential of a natural compound, 5-HTP, to enhance serotonin and promote well-being. In fact, a 2020 trial suggested that 5-HTP could help ease symptoms of depression – while other research has showcased its ability to encourage healthy eating habits. Let’s take a closer look at some of the possible benefits of 5-HTP. Serotonin-Producing 5-HTP May Reduce Unhealthy Food Cravings and Decrease Appetite 5-HTP, or 5-hydroxytryptophan, is made in the human body from tryptophan, an amino acid found in various foods, including poultry, milk, and bananas. (Unlike tryptophan, 5-HTP does not exist naturally in food. 5-HTP supplements are derived from an African plant known as Griffonia simplicifolia). After animal studies showed that 5-HTP appeared to reduce depression-induced excessive food intake, researchers began studying its effects on humans. In a 2017 study published in Brain and Behavior, participants were given either 5-HTP or vitamin C before undergoing MRI scans – and the results were fascinating. The researchers found that a “brain response for protein-rich foods” was more likely to occur in the 5-HTP group. In other words, the 5-HTP appeared to stimulate an inclination for healthier fare! (High-protein foods are more likely to help a person maintain a healthy weight than other choices, such as sugar- and fat-laden processed foods). Another controlled study showed that four weeks of using a 5-HTP oral spray led to greater feelings of fullness for overweight female participants, allowing them to decrease food intake and exhibit small but statistically significant reductions in body mass. The good news: While it’s by no means a “silver bullet” against obesity, 5-HTP may suppress appetite and reduce cravings for unhealthy foods, thereby helping to support a weight loss journey. 5-HTP Shows Promise in Enhancing Mood Low levels of serotonin (also known as the “feel-good” chemical) have been linked to depression and anxiety – leading some experts to speculate that serotonin-producing 5-hydroxytryptophan can help address these problems. In a recent controlled trial published in the European Journal of Neurology, researchers found that 50 mg of 5-HTP daily for a month caused significant improvements in depressive symptoms when compared to placebo. In fact, some researchers even maintain that 5-HTP may work as well as prescription medications to treat patients with mild-to-moderate depression. 5-HTP is believed to be particularly useful for patients who are resistant to pharmaceutical drugs or who have problems tolerating the side effects. Another “plus” for this calming compound is its ability to affect serotonin levels swiftly – unlike prescription antidepressants, which can take weeks to reach full effectiveness. “Catch More Zzzzs” – 5-HTP Boosts Levels of the “Sleep Hormone” Serotonin can be converted in the body into melatonin, a hormone important in regulating sleep. As 5-hydroxytryptophan spurs serotonin production, scientists believe it may enhance melatonin levels as well. While more research is needed, one promising 2018 study examined the effects of a combination of 5-HTP and GABA (gamma-aminobutyric acid, a neurotransmitter with calming effects). The team found that the combination helped to induce sleep, enhance sleep quality and support longer sleep duration – all encouraging findings for those struggling with insomnia and sleep disturbances such as night terrors, interrupted sleep, and sleepwalking. By the way, 5-HTP may also help reduce the frequency and severity of migraine headaches and relieve the muscle pain, sleep problems, and fatigue that can accompany fibromyalgia. 5-HTP May Soothe Jangled Nerves and Restore Restful Sleep Naturally Opt for a high-quality formulation from a reputable vendor. The label should clearly display a USP or NSF seal, which ensures that the product is free of impurities. Natural healers typically recommend 5-HTP amounts ranging from 50 mg to 400 mg a day – but consult your integrative physician before supplementing. (Important: Don’t attempt to treat depression, or any other condition, with 5-HTP unless you are under the guidance of a qualified physician. It may interact negatively with certain antidepressants and sedative medications, increasing the amounts of serotonin in the body to excessive levels). While researchers are still investigating the effects of 5-hydroxytryptophan, some users swear by its ability to promote sleep, regulate appetite, soothe anxiety and promote a calm, stable mood. This intriguing natural supplement certainly deserves further exploration. Sources for this article include: Healthline.com NIH.gov MedicalNewsToday.com CDC.gov To read the original article click here.

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