Puberty Before Age 10: A New ‘Normal’?

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By Dr. Mercola

Reaching puberty is a rite of passage that we’ve all been through, but children nowadays are reaching it earlier than ever before — a trend that has both health experts and parents alarmed.

Precocious puberty, which is the appearance of secondary sex characteristics like pubic hair or breast growth before age 8, or the onset of menarche before age 9, impacts at least 1 in 5,000 U.S. children, and the rate is on the rise.1

Even in the last three decades, children (particularly girls) are maturing at younger and younger ages (precocious puberty is 10 times more common in girls than in boys).

Puberty, Once the Norm at Age 15, Now Occurring in 7-, 8- and 9-Year-Olds

In the 19th century the onset of menstruation occurred around the age of 15. Now the average age of the first period, or menarche, is around 12. The time during and before puberty is one of rapid development and change, which is why even months matter when it comes to first menstruation. Before menstruation, girls will show beginning signs of development, such as breast “budding” and growth of pubic hair.

These signs are now becoming unsettlingly common among 7-, 8- and 9-year-old girls, to the extent that many health care providers, rather than labeling these children with a diagnosis that something is wrong, have simply changed the definition of what’s normal… but is it really “normal” for girls to mature at such a young age?

There are more questions than answers in the case of precocious puberty, but what is certain is that girls are developing earlier than they have even 10, 20 or 30 years ago.

One study in the journal Pediatrics revealed that by age 7, 10 percent of white girls, 23 percent of black girls, 15 percent of Hispanic girls and 2 percent of Asian girls had started developing breasts, with researchers noting:2

“The proportion of girls who had breast development at ages 7 and 8 years, particularly among white girls, is greater than that reported from studies of girls who were born 10 to 30 years earlier.”

Early puberty can set the stage for emotional and behavioral problems, and is linked to lower self-esteem, depression, eating disorders, alcohol use, earlier loss of virginity, more sexual partners and increased risk of sexually transmitted diseases. There is also evidence that suggests these girls are at increased risk of diabetes, heart disease and other cardiovascular diseases, as well as cancer, later in life.

Environmental Chemicals a Likely Factor

Scientists have brought forth a number of potential explanations for the rising rates of early puberty, but one that deserves special attention is environmental chemicals, and particularly estrogen-mimicking, “gender-bending” chemicals that easily leach out of the products that contain them, contaminating everything they touch, including food and beverages.

As the featured New York Times article reported:

” …animal studies show that the exposure to some environmental chemicals can cause bodies to mature early. Of particular concern are endocrine-disrupters, like “xeno-estrogens” or estrogen mimics. These compounds behave like steroid hormones and can alter puberty timing.

For obvious ethical reasons, scientists cannot perform controlled studies proving the direct impact of these chemicals on children, so researchers instead look for so-called “natural experiments,” one of which occurred in 1973 in Michigan, when cattle were accidentally fed grain contaminated with an estrogen-mimicking chemical, the flame retardant PBB.

The daughters born to the pregnant women who ate the PBB-laced meat and drank the PBB-laced milk started menstruating significantly earlier than their peers.”

This is an extreme case, but the truth is we are all part of a “secret experiment” of sorts, because hormone-disrupting chemicals are all around us. Bisphenol A (BPA), an industrial petrochemical that acts as a synthetic estrogen, is found in our plastics and our tin can linings, in dental sealants and on cash-register receipts. Laboratory tests commissioned by the Environmental Working Group (EWG) detected BPA in the umbilical cord blood of 90 percent of newborn infants tested — along with more than 230 other chemicals. As written in the New York Times:

“One concern, among parents and researchers, is the effect of simultaneous exposures to many estrogen-mimics, including the compound BPA, which is ubiquitous.”

No one knows what happens when a developing fetus or young child is exposed to hundreds of chemicals, many of which mimic your body’s natural hormones and can trigger major changes in your body even as an adult, let along during the most rapid and vulnerable periods of development (in utero and as a young child).

BPA is, unfortunately, but one example. Others include phthalates, a group of industrial chemicals used to make plastics like polyvinyl chloride (PVC) more flexible and resilient. They’re also one of the most pervasive of the endocrine disrupters, found in everything from processed food packaging and shower curtains to detergents, toys and beauty products like nail polish, hair spray, shampoo, deodorants, and fragrances.

Other environmental chemicals like PCBs and DDE (a breakdown product of the pesticide DDT) may also be associated with early sexual development in girls. Both DDE and PCBs are known to mimic, or interfere with, sex hormones.

Perfluorooctanoic acid (PFOA), found in non-stick cookware, also falls into this dangerous category, as does fluoride, which is added to the majority of public water supplies in the United States. Research showed that animals treated with fluoride had lower levels of circulating melatonin, as reflected by reduced levels of melatonin metabolites in the animals’ urine. This reduced level of circulating melatonin was accompanied — as might be expected — by an earlier onset of puberty in the fluoride-treated female animals.

These Chemicals Also Increase Your Risk of Cancer and Heart Disease

If a chemical is capable of influencing the rate of your reproductive development, it stands to reason that it would be capable of influencing other hormone-sensitive growth processes as well, and this is indeed the case.

For instance, new research has detected the presence of paraben esters in 99 percent of breast cancer tissues sampled.3 Parabens are chemicals with estrogen-like properties, and estrogen is one of the hormones involved in not only puberty but also the development of breast cancer. They are widely used in household products such as:

Deodorants and antiperspirants

Shampoos and conditioners

Shaving gel


Lotions and sunscreens

Make-up / cosmetics

Pharmaceutical drugs

Food additives

Recent research has also confirmed the existence of a previously unknown class of cancer-causing estrogen-mimicking compounds: metals. Yes, a broad range of metals have been shown to act as “metalloestrogens” with the potential to add to the estrogenic burden of the human body, thereby increasing the risk of breast cancer and also possibly early puberty. The following metals, which are added to thousands of consumer products, including vaccines, have been identified as being capable of binding to cellular estrogen receptors and then mimicking the actions of physiological estrogens:4















Data from a long-running British health survey, meanwhile, has shown that if you have high levels of the chemical BPA in your urine, you may be at an increased risk of heart disease. Some of the greatest concern surrounds early-life, in utero exposure to BPA, which can lead to chromosomal errors in your developing fetus, causing spontaneous miscarriages and genetic damage. But evidence is also very strong showing these chemicals are influencing adults and children, too, and leading to decreased sperm quality, early puberty, stimulation of mammary gland development, disrupted reproductive cycles and ovarian dysfunction, obesity, cancer and heart disease, among numerous other health problems.

Avoiding Hormone-Disrupting Substances is Crucial for Children and Adults Alike

While young girls may show obvious signs of exposure to hormone-disrupting substances via early puberty, other signals are more insidious and may not show up until a disease is already present. Here are 11 measures you can implement right away to help protect yourself and your children from common toxic substances that could cause precocious puberty and other long-term health problems:

  1. As much as possible, buy and eat organic produce and free-range, organic meats to reduce your exposure to added hormones, pesticides and fertilizers. Also avoid milk and other dairy products that contain the genetically engineered recombinant bovine growth hormone (rBGH or rBST)
  2. Eat mostly raw, fresh foods. Processed, prepackaged foods (of all kinds) are a major source of soy and chemicals such as BPA and phthalates.
  3. Store your food and beverages in glass rather than plastic, and avoid using plastic wrap and canned foods (which are often lined with BPA-containing liners).
  4. Use glass baby bottles and BPA-free sippy cups for your little ones.
  5. Make sure your baby’s toys are BPA-free, such as pacifiers, teething rings and anything your child may be prone to suck on.
  6. Only use natural cleaning products in your home to avoid phthalates.
  7. Switch over to natural brands of toiletries such as shampoo, toothpaste, antiperspirants and cosmetics. The Environmental Working Group has a great safety guide to help you find personal care products that are free of phthalates, parabens and other potentially dangerous chemicals.
  8. Avoid using artificial air fresheners, dryer sheets, fabric softeners or other synthetic fragrances, many of which can also disrupt your hormone balance.
  9. Replace your non-stick pots and pans with ceramic or glass cookware.
  10. When redoing your home, look for “green,” toxin-free alternatives in lieu of regular paint and vinyl floor coverings.
  11. Replace your vinyl shower curtain with one made of fabric.
  12. Avoid non-fermented soy, especially if you’re pregnant and in infant formula.

Theo Colburn’s book Our Stolen Future is a great source for further investigation as it identifies the numerous ways in which environmental pollutants are disrupting human reproductive patterns. I believe it is one of the best resources on this topic and highly recommend it.

Vitamin D Also Linked to Early Puberty

It has been suggested that girls who live closer to the equator start puberty at a later age than girls who live in Northern regions. Since this indicates a potential connection with sun exposure, researchers decided to investigate whether vitamin D was, in fact, related. Upon measuring vitamin D levels in 242 girls aged 5-12, researchers from the University of Michigan School of Public Health found that those who were deficient were twice as likely to start menstruation during the study period as those with higher levels.5

Specifically, among the vitamin-D-deficient girls, 57 percent started their period during the study, compared to 23 percent with adequate vitamin D. However, researchers defined adequate vitamin D as ≥ 30 ng/mL, which is actually still a deficiency state! For optimal health, vitamin D levels should be a minimum of 50 ng/mL, which means the number of vitamin-D-deficient girls with early puberty was probably much higher than the study reported.

The earlier you enter puberty, the longer you’re exposed to elevated levels of the female hormone estrogen, which is a risk factor for certain cancers such as breast cancer. This has been the primary “link” between early puberty and cancer that has been explored, but it’s important to understand that vitamin D deficiency is also a major risk factor for cancer, heart disease and many other diseases. So it could be that some of the increased risks that come from early puberty are linked to low vitamin D levels.

What You Should Know About Obesity, Stress and Exercise

Obesity (which exposes girls to more estrogen because estrogen is both stored and produced in fat tissue) is another likely factor in early puberty. The New York Times reported:

“As Robert Lustig, a professor of clinical pediatrics at the University of California, San Francisco’s Benioff Children’s Hospital, explains, fatter girls have higher levels of the hormone leptin, which can lead to early puberty, which leads to higher estrogen levels, which leads to greater insulin resistance, causing girls to have yet more fat tissue, more leptin and more estrogen, the cycle feeding on itself, until their bodies physically mature.”

As for stress, this, too, has been linked to early puberty, with girls whose parents divorced when they were between 3- and 8-years-old significantly more likely to experience precocious puberty. “Evolutionary psychology offers a theory,” the New York Times reports. “A stressful childhood inclines a body toward early reproduction; if life is hard, best to mature young. But such theories are tough to prove.” Interestingly, in addition to avoiding environmental chemicals, obesity and stress, and optimizing your vitamin D, regular exercise appears to be one of the best known ways to help prevent early puberty.

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Task Force Tells Women to Stop Doing This (No, Not Mammograms This Time)

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By Dr. Mercola

The US Preventive Services Task Force recently published its draft recommendations on hormone replacement therapy1.

While the task force has previously sparked controversy with its recommendations for breast cancer and PSA prostate cancer screening, their recommendations for hormone replacement therapy for menopausal women taking hormones to prevent chronic disease has been met with little resistance.

The group is changing its recommendations for menopausal women who use hormone therapy, either estrogen alone, or in combination with progestin to prevent heart disease, osteoporosis, and cognitive decline.

They are accepting public comments on the draft until June 26, at which point the group will decide whether to make the draft recommendations final. According to a recent report by CNN2:

“… The task force recommendations “are aimed at older women, who are generally healthy asking, ‘If I take a pill a day, will I prevent a heart attack?” [Dr. Carolyn] Crandall [professor of medicine at the David Geffen School of Medicine at UCLA] said.

… In the face of pretty good evidence, the balance of potential benefits and potential harms leads us not to recommend the use of these therapies,” said Dr. Kirsten Bibbins-Domingo, a task force member.

The proposed recommendations do not apply to women younger than 50 who have undergone surgical menopause or who are taking hormone therapy to manage menopausal symptoms such as hot flashes, according to the panel.

… “The balance of benefits or harms may be different with young women, so you can’t say this absolutely applies to younger women making hormone therapy decisions,” Crandall said.”

HRT as Preventive Strategy against Chronic Disease Not Supported by Data

The task force based their new recommendation on a recent review of the results from nine clinical trials published over the past decade3. The main question the group sought to answer was whether or not hormone replacement therapy (HRT) should be used by otherwise healthy menopausal women “to prevent a hypothetical future health event such as heart disease or cognitive decline.” Alas, according to the task force, “There is no evidence that the therapies would prevent those conditions4.

However, I would point out that this analysis is based on the use of synthetic hormones, not bioidenticals, which I’ll discuss more in a moment. That said, according to the featured CNN article:

“Years ago, in addition to providing relief for menopause symptoms, hormone therapy was thought to offer protection against cardiovascular problems, osteoporosis and dementia, so doctors routinely prescribed it to otherwise healthy women. That practice fell out of favor about 10 years ago when a large clinical trial — the Women’s Health Initiative — designed to confirm these hypotheses was halted early. Women involved in that trial were actually at higher risk for many of the problems that hormone therapy was supposed to prevent.”

Indeed, many large-scale trials, including the Women’s Health Initiative, have indicated that taking estrogen alone, or the combination of estrogen and progestin, actually increased women’s chances of developing strokes, dementia, deep vein thrombosis, urinary incontinence and gallbladder disease.

“The bottom line is clinicians must take all clinical parameters into account for the patient and prescribe the lowest dose for the shortest duration of time,” said Dr. Joseph Sanfilippo, vice chairman of reproductive sciences at Magee-Women’s Hospital in Pittsburgh, in an e-mail to CNN5.”

There are Better Ways to Prevent Heart Disease than HRT

Heart disease prevention is indeed an important concern, but there are far more effective, not to mention safer ways to prevent heart attacks and strokes than using HRT. Key lifestyle strategies that will help protect your heart naturally include:

  • Boost your good cholesterol and lower your triglyceride levels: Many people strive to reduce their cholesterol levels to protect their heart, but high levels of good (HDL) cholesterol are believed to be protective against heart disease. Meanwhile, high triglycerides are an incredibly potent risk factor. In combination, high triglycerides and low HDL levels are an even bigger risk; this ratio is even more important to your heart health than the standard good vs. bad cholesterol ratio.
  • In fact, one study found that people with the highest ratio of triglycerides to HDL had 16 times the risk of heart attack as those with the lowest ratio of triglycerides to HDL.

    You can increase your HDL levels by exercising and getting plenty of omega-3 fats like those from krill oil. Triglycerides are easily decreased by exercising and avoiding grains and sugars in your diet.

  • Get enough high quality animal based omega-3 fats: Regularly taking a high-quality animal-based omega-3 supplement such as krill oil is one of the easiest ways to help promote your heart health.
  • Check your iron levels: If you have excessive levels in your body you are at risk of major oxidation, or premature aging as excessive iron acts as a catalyst to increase your free radical formation though excessive oxidation. Excess iron will also increase your risk of heart disease and cancer. If you are a man, or a woman in menopause, you should get your iron levels tested and, if they’re too high, take steps to reduce them. The simplest way to reduce your iron levels is by donating blood.
  • Normalize your insulin levels: Elevated insulin levels can lead to insulin resistance, a major risk factor for heart disease. Carefully avoiding sugar/fructose and grains, combined with regular exercise are the most effective strategies for getting your insulin levels back to normal.
  • Avoid FAKE Estrogens. These are also called xenoestrogens and are pervasive in modern culture. Non-organic foods are loaded with pesticides and herbicides that have potent xenoestrogenic activity. Addtiionally, plastics have BPS and phthalates and many cosmetics have parabens. It is wise to avoid all of these items as they are potent estrogenic influences which can increase a woman’s risk of breast cancer.
  • Keep your mouth healthy: Gum disease can trigger heart attacks, so make sure you keep your teeth, gums and mouth clean.

Should You Treat Menopause with HRT?

As stated earlier, the panel’s recommendation to avoid HRT is only directed to menopausal women who are using synthetic hormones as a preventive measure. It does not apply to women who are managing symptoms of menopause (such as hot flashes, mood swings, and depression), or younger women who take hormones due to having their ovaries removed (surgically-induced menopause).

In these cases, hormone therapy can still be useful, and in the case of surgically-induced menopause, a necessity. However, it’s a complex topic, and synthetic hormone replacement does have its risks, which is why I do not recommend using them. There are a number of different kinds of estrogen: Pharmaceutical estradiol comes from plant molecules modified in a lab, while Premarin and Prempro contain potent horse estrogens that are manufactured from the urine of pregnant mares. All of these are synthetic versions that have their share of side effects.

Can You Believe Drug Companies Used to Pay Me to Promote HRT?

Yes, at one time I was part of the dark side. Many of you may not know this about me, but after finishing my medical residency training in the mid-80s, I was actually a paid speaker for the drug companies. I got paid to fly around the country to lecture physicians about estrogen replacement therapy. At the time, I was convinced it was an ideal strategy for menopausal women because I was manipulated and deceived by the overwhelming “evidence” that was published in the respected peer-reviewed medical journals.

Only decades later would I finally understand the massive corruption and collusion between the drug companies, medical journals and federal regulatory agencies that provided the illusion of scientific legitimacy when the real primary purpose was to increase their sales.

I still believe replacing your hormones can be a good strategy. But in my journey of learning about and truly coming to understand health, I’ve realized that using synthetic hormones, and even natural hormones from animals, is not a wise choice.

A much better alternative is to use bioidentical hormones. These are natural hormones that are “bioidentical” to the ones your body produces. The bioidentical that is prescribed 80 percent of the time is estriol. It’s natural, not a drug, and you get it at compounding pharmacies. It has been used safely for decades, and I believe it’s particularly useful when your ovaries have been removed or you’ve had a hysterectomy. 

The Ideal Way to Administer Bioidentical Hormones

Keep in mind that when it comes to administering bioidentical hormones, some delivery methods are clearly superior to others. Oral supplementation is perhaps your worst option, as your liver processes everything in your digestive tract first, before it enters your bloodstream. Any method that bypasses your liver will therefore be more effective. Hormone creams are one common alternative that achieves this. However, since hormones are fat-soluble, they can build up in your fatty tissues and lead to having too much in your body. This in turn can disrupt other hormones. It’s also near impossible to accurately determine the dose when using a cream.

That is why I STRONGLY recommend trans mucosal administration. Please
listen to my interview at the top of the article with Dr. Wright in
which we discuss this near the end of the interview. 


What to do BEFORE Taking Hormones for Menopause

Natural bioidentical hormones can offer relief from menopausal symptoms, but I recommend not using them as your first go-to option. Treating hormone imbalances requires a whole-body approach; the best approaches are often preventive and involve diet, exercise and other lifestyle-based strategies.

For instance, both estrogen and progesterone are necessary in the female cycle, and their balance is key for optimal health. Many premenopausal women have an imbalance of these hormones. And if you have insufficient levels of progesterone to counter excessive estrogen, this imbalance can be further exacerbated by chronic stress. Therefore, your answer might not necessarily lie in using hormones, but rather addressing your stress levels so that your body can normalize your hormone levels naturally.

Likewise, a healthful diet, low in processed foods (which are high in health-harming sugars/fructose, grains, genetically engineered ingredients, trans fats, processed salt, and other chemical additives) and high in whole organic foods, along with regular exercise, can go a long way to keeping your hormones balanced as you age. It’s important to realize that processed foods—all those refined carbohydrates, and processed and heated fats, all serve to raise your estrogen to abnormal levels—as much as twice the normal, which are maintained for the better part of the adult lives of most American women.

This is a MAJOR contributing cause of menopausal symptoms in the first place. Additional strategies you can try before resorting to bioidentical hormones include:

  • Phytoestrogens: Consuming plenty of phytoestrogens (plant-estrogens) such as licorice and alfalfa before menopause can also help moderate your day-to-day estrogen levels so that when menopause comes, the drop won’t be so dramatic. Just don’t make the mistake of using unfermented soy, which can wreak havoc on your health in a number of different ways.
  • Optimize your vitamin D levels: This is a must for gene regulation and optimal health. For more information, I recommend you watch my one-hour video lecture on this essential nutrient.
  • Polyphenols: Certain polyphenols have also been shown to have some HRT-like benefits without the drawbacks, and are associated with a lowered risk of heart disease. Royal Maca seems to be an amazing adaptogenic herbal solution for menopause that has helped many women. Be sure to avoid the inexpensive varieties, as they typically don’t work. If you chose this option make sure to obtain the authentic version from Peru.
  • Animal-based omega-3 fat: You’ll also want to get plenty high quality animal-based omega-3 fats, such as krill oil.
  • Black cohosh: Black Cohosh may help regulate body temperature and hot flashes. In many cases, these lifestyle strategies will be very effective in relieving menopausal symptoms, but in cases where it is not enough, bioidentical hormones may be able to help. However, you’ll want to make sure you get your hormonal levels checked properly before embarking on any kind of hormone supplementation program, and work with a knowledgeable health care practitioner who can guide you.


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Accutane Acne Drug Widely 'Overused' Says UK Dermatologist

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By Dr. Mercola

Up to 50 million Americans struggle with acne, making it the most common skin disorder in the United States.1

When it strikes during the teen years, it can lead to feelings of self-consciousness, embarrassment and depression. Many severe acne sufferers struggle with low self-confidence, feelings of alienation and social withdrawal as a result.

And it’s not only teens who are affected; one in five U.S. adults also suffers from acne, and for them the psychological toll is often no less severe.

Many are desperate for help to clear their skin, and if the typical face washes and topical treatments don’t work, they may gratefully accept a prescription for the acne drug Roaccutane (generic name, isotretinoin, and formerly sold as Accutane in the United States).

Isotretinoin (Formerly Sold as Accutane) Greatly Overused

This is an extreme step, given that isotretinoin is easily one of the most dangerous drugs ever made. Yet, incredibly it remains the industry standard for treating severe acne. One leading UK dermatologist even recently spoke out to say it is being greatly overused.

More than half a million people worldwide have been prescribed Roaccutane, despite the fact that it’s intended to be used only as a last resort (and even then its use is highly questionable). But UK dermatologist Tony Chu said that often Roaccutane is being offered far more than that:2

Roaccutane is grossly overused …I’ve seen patients who have been to see a local dermatologist to treat four of five spots and still been offered it … If you read the guidelines it should only be used for people who have severe acne.”

In the United States, it remains one of the most controversial drugs, and Swiss drugmaker Roche, manufacturer of Accutane, has spent most of this century in court defending itself against lawsuits from people whose health has been irreparably damaged by this menacing drug.

Inflammatory Bowel Disease, Suicide, Depression and More …

Roche has lost nine out of 13 lawsuits since 2007, and was ordered to pay more than $25 million in damages in 2010, plus another $18 million in 2012, to Accutane users who developed inflammatory bowel disease as a result of the drug. Due to generic competition and the exorbitant cost of defending personal injury lawsuits, Roche stopped selling the drug in June 2009.

However, the generic form of Accutane (isotretinoin) is no less deadly and remains available on the marketplace under the names Claravis, Sotret and Amnesteem. Aside from its links to inflammatory bowel disease, Accutane has been implicated as a cause of depression and suicide.

In 2004, brain scans showed that people taking Accutane suffer a 21 percent decrease in activity in the orbitofrontal cortex, a brain area known to mediate symptoms of depression.3 These brain changes may explain the depression, suicidal and aggressive behavior, and psychotic reactions reported by some Accutane users.

Is reducing your acne worth that? In light of this evidence and reports of suicide or suicide attempts associated with the use of isotretinoin, the U.S. Food and Drug Administration (FDA) stated:4

“All patients treated with isotretinoin should be observed closely for symptoms of depression or suicidal thoughts, such as sad mood, irritability, acting on dangerous impulses, anger, loss of pleasure or interest in social or sports activities, sleeping too much or too little, changes in weight or appetite, school or work performance going down, or trouble concentrating, or for mood disturbance, psychosis, or aggression.

…Patients taking isotretinoin may experience side effects including bad headaches, blurred vision, dizziness, nausea, vomiting, seizures, stroke, diarrhea, and muscle weakness. Additionally, serious mental health problems, such as depression and suicide, have been reported with isotretinoin use.”

Isotretinoin is a Category X Drug for Pregnancy – Guaranteed to Cause Birth Defects

Isotretinoin now has the strongest warning available for any drug category — and was given an FDA Pregnancy Category X rating, which means if you are taking isotretinoin and become pregnant, you are virtually guaranteed to be damaging your baby. Accutane is extremely teratogenic (causing damage to a fetus). According to the FDA:5

“If you are pregnant or may get pregnant, isotretinoin can cause birth defects, miscarriage, premature births, and death in babies.”

The risk is so well-established that anyone taking the drug must go through the FDA’s iPledge system, which was designed specifically to eliminate fetal exposure to this toxic drug. The system requires both the patient and the prescriber to enter in specific information on a monthly basis prior to the drug being dispensed. In the United States, a woman must:

  • Use two forms of effective contraception simultaneously for one month before, during, and for one month after isotretinoin therapy.
  • Have two negative urine or blood (serum) pregnancy tests with a sensitivity of at least 25 mIU/ml before receiving the initial isotretinoin prescription (an additional pregnancy test must be taken with each month of additional therapy).

According to the FDA’s iPledge system:6

“There is an extremely high risk that severe birth defects will result if pregnancy occurs while taking isotretinoin in any amount, even for short periods of time. Birth defects which have been documented following isotretinoin exposure include abnormalities of the face, eyes, ears, skull, central nervous system, cardiovascular system, and thymus and parathyroid glands. Cases of IQ scores less than 85 with or without other abnormalities have been reported. There is an increased risk of spontaneous abortion, and premature births have been reported.

Documented external abnormalities include: skull abnormality; ear abnormalities (including anotia, micropinna, small or absent external auditory canals); eye abnormalities (including microphthalmia); facial dysmorphia; cleft palate. Documented internal abnormalities include: CNS abnormalities (including cerebral abnormalities, cerebellar malformation, hydrocephalus, microcephaly, cranial nerve deficit); cardiovascular abnormalities; thymus gland abnormality; parathyroid hormone deficiency. In some cases death has occurred with certain of the abnormalities previously noted.”

If a drug is this toxic to a developing fetus, it certainly does make you wonder how it could possibly be safe for any living creature. Indeed, in addition to teratogenic and psychological adverse effects, Accutane (isotretinoin) users have also reported the following negative effects:

Increased levels of triglycerides and cholesterol in your blood Increased liver enzyme levels and liver damage Erectile dysfunction
Headaches and brain swelling Disturbances of your central nervous system Seizures
Damage to skin and mucous membranes Premature epiphyseal closure Hyperostosis (excessive bone growth) and bone demineralization Neutropenia, agranulocytosis, and rhabdomyolysis (blood disorders)
Development of inflammatory bowel disease Damage to your eyes including cataracts Hearing impairment
Pancreatitis Heart attack and stroke Allergic vasculitis

Did You Know Acne Can be Treated Naturally?

The root cause of acne is most likely not bacteria or genetics, but environmental factors — particularly your diet. Acne is much less of a problem in non-Westernized societies, where refined carbohydrates, sugar and fructose are consumed in much lower amounts. Solid evidence exists that diets high in sugar and refined carbohydrates are the primary CAUSE of acne.

When you eat grain carbohydrates and sugar/fructose, it causes a surge of insulin and an insulin-like growth factor called IGF-1 in your body.7 This can lead to an excess of male hormones, which cause your pores to secrete sebum, a greasy substance that attracts acne-promoting bacteria. Additionally, IGF-1 causes skin cells known as keratinocytes to multiply, a process that is also associated with acne.

Additionally, these very same foods — refined carbs, such as fructose, sugar and grains — will also increase inflammation in your body, which may trigger acne, and at the same time they will also wreak havoc on the makeup of your intestinal bacteria, which may also play a role.

This is why simply eliminating grains, sugars (particularly fructose), cereals, potatoes, corn, rice, pasta, processed foods, etc., radically improves acne for most people. Fruit contains a fair amount of fructose, so it should be consumed in very limited quantities if you are predisposed to acne. And fruit juices should be strictly avoided since the sugar is very concentrated in them. (Vegetable juices are great, though, especially green juices.)

Additionally, psychological stress may also alter the microflora in your intestines, which could therefore contribute to systemic inflammation that could exacerbate acne and other skin conditions. In one study, researchers noted:8

“Experimental studies show that psychological stress stagnates normal small intestinal transit time, encourages overgrowth of bacteria, and compromises the intestinal barrier. SIBO [small intestinal bacterial over growth] is strongly associated with depression and anxiety, while eradication of SIBO improves emotional symptoms.

Although the frequency of SIBO in acne vulgaris has not yet been investigated, a recent report indicates that SIBO is 10 times more prevalent in those with acne rosacea vs. healthy controls. Correction of SIBO leads to marked clinical improvement in patients with rosacea.”

It’s actually well proven that stress can aggravate acne. One study involving college students found a connection between acne flare-ups and stress from final exams.9 Researchers found that subjects who had the most stress during examination periods also had the worst acne outbreaks, suggesting emotional stress from external sources is a significant factor. While it has been argued that the stress associated with acne is an effect of acne rather than a cause, the above researchers believe this evidence proved otherwise — that it’s the stress that is exacerbating the acne, not vice versa.

Ditch the Drugs and Try This Instead

No one wants to live with acne, but that doesn’t mean you have to resort to toxic drugs to clear your skin. Remember, your complexion is a reflection of your overall health. Don’t forget to incorporate these essential factors into your acne-busting plan:

  • Sugars/Fructose and Grains: This is probably the single most important step you can take to improve your skin health. If you can eliminate all sugars, fructose and grains for a few weeks there is a major likelihood you will notice rapid improvement in your complexion. Be sure to check out my nutrition plan for a simple guide on how to eat right for healthy skin and overall health.
  • Water: Drink plenty of fresh, pure water every day. Hydrating your body facilitates cell growth and regeneration, elimination of wastes, and sloughing away dead skin cells. Hydration will also improve your skin tone.

    Every day, drink enough water so that your urine is a pale yellow color. If your urine is bright yellow, you probably need to drink more water (unless you take B vitamins, which themselves turn urine bright yellow).

  • Exercise: Getting plenty of high-intensity exercise helps your body flush out toxins, including those in your skin’s pores. Plus, exercise is vitally important to all other aspects of your heath. If you happen to have access to an infrared sauna, this can be helpful too, because the more you sweat, the more you flush unwanted debris and contaminants out of your pores.
  • Sleep: Did you know that a good night’s sleep can decrease your stress and lead to clearer skin? Your body’s main time for healing and rebuilding is at night while you sleep, and this applies to your skin. Sleep is also required for good energy and mood.
  • Proper balance of bacteria: This is especially important if you have been on antibiotics, because those drugs indiscriminately kill off the beneficial bacteria in your gut, without which you cannot have a strong immune system. You can reestablish your bacterial balance by incorporating naturally fermented/cultured foods into your diet and/or taking a high-quality probiotic supplement.
  • Vitamin D: This important nutrient is crucial for maintaining a healthy immune response, and most people are deficient in it. Without adequate vitamin D, your body cannot control infection, in your skin or elsewhere. Exposing large areas of your skin to appropriate amounts of sunshine is the best way to optimize your vitamin D levels, or alternatively use a safe tanning bed. You should expose your skin until you just barely begin turning pink, which indicates you’ve generated the optimal amount of vitamin D for the day.
  • If you don’t have access to regular UV exposure, the last option is an oral vitamin D3 supplement, accompanied by regular monitoring of your vitamin D levels with a blood test.

  • Address your stress: My favorite tool is the Emotional Freedom Technique, or EFT. EFT involves tapping your body’s energy meridians with the tips of your fingers to clear emotional blocks, thus restoring balance to your mind and body. EFT is a powerful de-stressing technique that is easy for adults and children to learn. It can even relieve physical complaints such as chronic pain, allergy symptoms, and more. You can also add in other proven stress-busters, such as yoga and meditation.

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Cellular Senescence is Important in Zebrafish Fin Regrowth

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Species such as salamanders and zebrafish are capable of regrowing lost limbs, fins, and organ tissue without scarring, leading to a fully functional replacement. Regeneration from injury is in general a complex dance of different cell types: immune cells, stem cells, somatic cells. Further, senescent cells play an important part in this process. In response to injury some cells enter a senescent state and their inflammatory secretions help to coordinate the process of regrowth. The senescent cells either self-destruct or are destroyed by the immune system shortly thereafter – though, of course, this process of clearance is not completely efficient, and that inefficiency has sizable consequences over the long term. That some senescent cells linger, and in increasing numbers as the immune system falters with age, is a contributing cause of degenerative aging.

Research into the details of proficient regeneration in a variety of species points to significant differences in the behavior of senescent cells and their interactions with other cell types. Salamanders, for example, exhibit highly efficient clearance of senescent cells by immune cells following regeneration. A prehaps similar situation is present in African spiny mice, which are capable of more extensive regeneration than is the case for most mammals. In today’s open access research, the focus is on zebrafish, and the authors show that removal of a sizable fraction of senescent cells via senolytic treatment impairs regrowth but doesn’t prevent it. It would be interesting to see the outcome of complete clearance of senescent cells.

Cell senescence contributes to tissue regeneration in zebrafish

Cellular senescence is a terminal cell response consisting on the implementation of a permanent cell cycle arrest and the acquisition of a secretory phenotype with cell-to-cell communication properties. Exhaustion of the proliferative capacity of the cell leads to senescence, and the accumulation of these damaged cells in tissues from old individuals is considered a key element in the process of aging. Despite this detrimental effect, the senescence response has a beneficial side protecting damaged cells from proliferating. This is considered the basis of its tumor-suppressive function. The recent identification of developmentally programmed cell senescence during embryogenesis expanded our view of the positive activities of this response. Senescence during development promotes cell turnover, tissue remodeling, and, paradoxically, growth. A similar positive pro-morphogenetic activity for cell senescence has been suggested to operate during skin wound healing in mice and during limb regeneration in salamanders. Senescent cells seem to appear at wound sites after injury to help promote optimal wound healing.

Here, we decided to evaluate the senescence response in the context of tissue injury using an animal model of complex tissue regeneration, the zebrafish. To study senescence after tissue damage, we amputated the pectoral fin of adult fish (around 1 year old) at approximately 50% of its length and followed regeneration with time. We stained fins for senescence-associated beta-galactosidase (SAbetaGal), the most widely used marker of senescence, after 8, 16, or 30 days postamputation (dpa), a time point in which fins were completely regenerated. Fins at 8 dpa showed intense blue staining compared with light blue at 16 dpa and completely absent staining at 30 dpa. We observed that 8 dpa was the time point that produced a stronger SAbetaGal reaction and this activity was restricted to the distal part of the fin, the area where regeneration takes place. These results support the notion of a transient induction of cell senescence during fin regeneration.

To directly assess the role of senescence induction during fin amputation, we decided to induce the removal of these senescent cells from amputated fins. For this, we treated fish for 48 or 72 hr with ABT-263 (Navitoclax), a senolytic compound that by inhibiting the Bcl-2 antiapoptotic family of proteins triggers specifically the death of the senescent cell. ABT-263 treatment caused a reduction in SAbetaGal staining and a concomitant induction of apoptosis in the regenerating area. We determined the regenerative capacity by measuring the length of regenerate at 8 dpa in fish treated with ABT-263. This analysis revealed that the removal of senescent cells by ABT-263 treatment clearly impaired regeneration, with amputated fins in fish treated with ABT-263 showing a clear reduction in the length of regenerate compared with the one reached in control animals.

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Rapamycin Prevents Deterioration in Brain Circulation in Aged Rats

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The mTOR inhibitor rapamycin is well known to slow aging in animal models. As for most of the methods shown to achieve this goal in short-lived species, upregulation of cellular maintenance processes such as autophagy features prominently in the changes produced by the drug. Every one of these approaches that produce sweeping changes in cellular metabolism and a general slowing of age-related decline provides the research community with an essentially unlimited range of projects to undertake when it comes to assessing specific metrics of aging and how they are affected.

Here, researchers look at how rapamycin affects age-related deterioration in blood circulation in the brain. There are many reasons why this might decline: a weakened or failing heart; loss of capillary network density; narrowing of blood vessels due to atherosclerosis; and so forth. The brain is an energy-hungry organ, and any reduction in the supply of oxygen and nutrients will have detrimental effects on tissue function, contributing to the onset of neurodegeneration.

Cerebrovascular dysfunction and cognitive decline are highly prevalent in aging, but the mechanisms underlying these impairments are unclear. Cerebral blood flow decreases with aging and is one of the earliest events in the pathogenesis of Alzheimer’s disease (AD). We have previously shown that the mechanistic target of rapamycin (mTOR) drives disease progression in mouse models of AD and in models of cognitive impairment associated with atherosclerosis, closely recapitulating vascular cognitive impairment. In the present studies, we sought to determine whether mTOR plays a role in cerebrovascular dysfunction and cognitive decline during normative aging in rats.

Using behavioral tools and MRI-based functional imaging, together with biochemical and immunohistochemical approaches, we demonstrate that chronic mTOR attenuation with rapamycin ameliorates deficits in learning and memory, prevents neurovascular uncoupling, and restores cerebral perfusion in aged rats. Additionally, morphometric and biochemical analyses of hippocampus and cortex revealed that mTOR drives age-related declines in synaptic and vascular density during aging. These data indicate that in addition to mediating AD-like cognitive and cerebrovascular deficits in models of AD and atherosclerosis, mTOR drives cerebrovascular, neuronal, and cognitive deficits associated with normative aging.

Thus, inhibitors of mTOR may have potential to treat age-related cerebrovascular dysfunction and cognitive decline. Since treatment of age-related cerebrovascular dysfunction in older adults is expected to prevent further deterioration of cerebral perfusion, recently identified as a biomarker for the very early (preclinical) stages of AD, mTOR attenuation may potentially block the initiation and progression of AD.


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The Gut Microbiome in Neuroinflammation and Alzheimer's Disease

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The microbial populations of the gut influence and are influenced by the state of the immune system. They also have effects on tissue function throughout the body via secreted compounds such as butyrate, mediating some of the effects of diet on long-term health. These microbes change with age, losing beneficial populations and gaining harmful populations that contribute to chronic inflammation. These changes are far from fully explored at the present time, but may have effects on health that rival those resulting from regular exercise. In this open access review, researchers discuss the influence of gut microbes on chronic inflammation of the brain, and the development of neurodegenerative conditions such as Alzheimer’s disease.

Alzheimer’s disease (AD) is a complex, multi-factorial disease affecting various brain systems. This complexity implies that successful therapies must be directed against several core neuropathological targets rather than single ones. The scientific community has made great efforts to identify the right AD targets beside the historic amyloid-β. Neuroinflammation is re-emerging as determinant in the neuropathological process of AD. A new theory, still in its infancy, highlights the role of gut microbiota in the control of brain development, but also in the onset and progression of neurodegenerative diseases.

Bidirectional communication between the central and the enteric nervous systems, called gut-brain axes, is largely influenced by gut microbiota and the immune system is a potential key mediator of this interaction. Growing evidence points to the role of gut microbiota in the maturation and activation of host microglia and peripheral immune cells. Several recent studies have found abnormalities in gut microbiota (dysbiosis) in AD populations. These observations raise the intriguing question whether and how gut microbiota dysbiosis could contribute to AD development through action on the immune system and whether, in a therapeutic prospective, the development of strategies preserving a healthy gut microbiota might become a valuable approach to prevent AD.


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How to Start a Biotech Company in the Longevity Industry

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Based on discussions with various folk at scientific and industry conferences earlier this year, regarding whether or not our rejuvenation research, development, and advocacy community is challenging to approach and understand as an outsider, I recently put together an introductory document for entrepreneurs entitled
How to Start a Biotech Company in the Longevity Industry (PDF). Given my experiences, it is primarily aimed at entrepreneurs with previous experience in other industries, who are now interested in helping to treat aging as a medical condition and there by greatly improve the human condition.

The young and rapidly growing longevity industry encompasses the clinical development of rejuvenation therapies, such as senolytic therapies to clear senescent cells from old tissues, or the thymic regeneration project taking place at Repair Biotechnologies, the company I founded with Bill Cherman last year. It also includes initiatives that can only modestly slow aging, such as mTOR inhibitor and NAD+ upregulation programs. All told there are around 100 companies in the industry as of late 2019, of which perhaps a fifth could be argued to be working on programs relevant to the SENS damage repair view of aging, and which thus might lead to rejuvenation therapies. Clearly we still have some way to go in persuading people that only damage repair and rejuvenation is worth the effort, when looking at the long term and the big picture.

Yes, once the sizable expense of clinical development has been expended, it will be a good deal for older patients to be able to spend $60 a month on a drug that halves the rate of influenza infection – this more or less describes an early use case for an mTOR inhibitor, based on the work taking place at resTORbio. But the cost of clinical development of an mTOR inhibitor and a senolytic are pretty much the same, and the senolytic is vastly, enormously more beneficial, based on the animal data to date. It is transformative, where mTOR inhibitors produce only incremental gains. No-one should be choosing to work on projects that can only produce small gains, when there are many alternatives that have the potential to produce large gains, and yet most people in the industry are doing just that.

This is not why I wrote an introduction to starting a biotech company in the longevity industry. I wrote it because I was having the same conversation with interested entrepreneurs from other industries over and again at conferences. The longevity industry is in an interesting state at the moment: there is far more funding than there are early stage companies to absorb it, there are not enough entrepreneurs, and there are scores (at the very least) of scientific programs relevant to the treatment of aging as a medical condition that are ready for clinical translation, but lacking anyone to carry out the work. That there is so much venture funding and excitement is attracting interest from the broader entrepreneurial community, but not rapidly or robustly enough. It takes time to find out what questions one should even be asking when coming into the longevity industry completely naive.

Thus the need for more introductory documents, and thus this introductory document. Because it comes from me, it is intended not just to help newcomers find their way, but also to point out that working on rejuvenation is far, far more beneficial for all parties concerned than is the case for work on slowing aging. The first draft of the document is available as a PDF. Hopefully it proves useful, and, as always, feedback is welcome.

How to Start a Biotech Company in the Longevity Industry (PDF)

You are an entrepreneur who wishes to start a longevity industry biotech startup, but your experience to date is in a different industry. This document is an initial primer and guide to help you get started. New classes of therapy, targeting the mechanisms of aging, have the potential to prevent and reverse all age-related disease, and greatly extend healthy human lifespan. The first rejuvenation therapies are already under clinical development in numerous startup companies. This new longevity industry is growing exceptionally rapidly. Venture funding for longevity startups is increasing enormously year over year. Yet there are far too few entrepreneurs and new startups in comparison to the available funding. Your arrival will be welcomed: this is a friendly, and close-knit community.

You are entrepreneurial. You have heard the buzz about the new longevity industry: the rapid growth in funding, the numerous billionaires becoming involved, the new approaches to medicine that are targeting the mechanisms of aging to prevent and reverse the diseases and frailty of old age. You want to get involved, to start a company, to do something about aging … to change the world for the better. But how? Whatever your past industry, here you must be the business co-founder. Life science and its application to biotechnology is a vast, complex, intimidating field. Aging is its own highly specialized portion of that field. You need an understanding sufficient to identify a project to work on; you need a scientific co-founder; you need to know the investors and the movers and shakers. Where to even start?

This document is a starting point. We hope that it helps.

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Delivery of MALAT1 in Exosomes as a Treatment for Osteoporosis

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Bone is not a static tissue. It is constantly remodeled, broken down by osteoclast cells and built up by osteoblast cells. The loss of bone mass and strength with age, osteoporosis, is the result of an imbalance in the activities of osteoclasts and osteoblasts, too much destruction and too little creation. This imbalance, as for all aspects of aging, is the result of many deeper overlapping layers of cause and effect, not fully mapped and understood. Thus most approaches to therapy tend to involve ways to force greater activity of osteoblasts or suppress the activity of osteoclasts, rather than delving in search of root causes. The open access paper here is an example of this type of work, outlining an approach to stimulate greater osteoblast activity in mice.

In recent years, promising therapeutic approaches to treat osteoporosis are mainly focused on targeting the functions of skeletal stem cells and osteoblasts. A more detailed understanding of bone biology has led to the identification of novel therapeutic targets with enhanced molecular insights into the communication between bone-forming osteoblasts and bone-resorbing osteoclasts as well as the orchestrating signaling network. Thus, it is necessary to develop new approaches to stimulate osteoblast activity. In the present study, we demonstrate that bone marrow stem cell (BMSC) derived exosomes carrying the long non-coding RNA (lncRNA) MALAT1 could effectively stimulate the osteoblast activity. Our results highlighted the potential of exosomal MALAT1 to prevent osteoporosis in mouse models.

A key finding of the current study indicated that BMSCs-derived exosomal MALAT1 could potentially promote osteoblast activity. Exosomes could actively transport and transfer information between miRNAs, proteins, and mRNAs to target cells, thus affecting their behaviors and strongly modifying the entire microenvironment. Consistent with previous reports, we observed the protective role of exosome-mediated delivery of MALAT1 in disease. Furthermore, we detected that the upregulation of MALAT1 could attenuate the symptoms of osteoporosis in mice. Existing literature has suggested that lncRNAs play critical roles in the initiation and pathogenesis of osteoporosis. For instance, a recent study demonstrated that lncRNA MEG3 suppressed the osteogenic differentiation of mesenchymal stem cells in postmenopausal osteoporosis.

Our study provides evidence that BMSC-derived exosomal MALAT1 may contribute to enhanced osteogenic activity and alleviated symptoms of osteoporosis in the mouse model by acting as a miR-34c sponge to upregulate SATB2 expression. These results provide a broader understanding of the pathogenesis of osteoporosis as well as novel therapeutic strategies for its treatment.


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Senescent Cells Mediate the Incidence of Periodontitis in Diabetic Patients

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Insofar as either type 1 diabetes or type 2 diabetes increase the burden of senescent cells, we might say that the condition literally accelerates aging. The accumulation of lingering senescent cells is a contributing cause of aging; these errant cells disrupt tissue function and produce the characteristic profile of chronic inflammation known as inflammaging via a potent mix of secreted molecules and vesicles. Diabetic patients suffer more and worse gum disease, periodontitis, than their healthy peers, and researchers here show that hyperglycemia leads to increased numbers of senescent cells in gum tissue, causing all of the expected downstream consequences resulting from inflamed gums.

Inflammaging was recently affiliated with the progression of diabetic complications. Local cellular senescence together with senescence-associated secretory phenotype (SASP) are the main contributors to inflammaging. However, little is known about their involvement in diabetic periodontitis. Gingiva is the first line of host defense in the periodontium, and macrophages are key SASP-carrying cells. Here, we explored the molecular mechanism by which hyperglycemia drives the inflammaging in the gingival tissue of diabetic mice and macrophages.

We demonstrated that hyperglycemia increased the infiltrated macrophage senescence in gingival tissue of diabetic mice. Simultaneously, hyperglycemia elevated the local burden of senescent cells in gingival tissue and induced the serum secretion of SASP factors in vivo. Moreover, in vitro, high glucose induced macrophage senescence and SASP factors secretion through phosphorylation of NLRC4, which further stimulated the NF-κB/Caspase-1 cascade via IRF8-dependent pathway.

Deletion of NLRC4 or IRF8 abolished hyperglycemia-induced cellular senescence and SASP in macrophages. In addition, we found that treatment with metformin inhibited NLRC4 phosphorylation and remarkably decreased cellular senescence and SASP in the context of hyperglycemia. Our data demonstrated that hyperglycemia induces the development of inflammaging in gingival tissue and suggested that NLRC4 is a potential target for treatment of diabetes-associated complications.


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Research Update: Miso Health Benefits

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Research Update: Miso Health Benefits
Dayna Dye

Do you order miso soup with your sushi? Turns out, this may be a healthful habit. Blog readers may recall a 2015 post that we published titled the “Magic of Miso” which reported the various benefits of this Japanese staple. Miso continues to reveal its benefits in both popular and scientific literature. Here is More on Miso!

What is Miso?

Miso, a fermented paste of soybeans, has a long history of culinary use among the Japanese, who are known for their longevity. The beans are fermented with koji (Aspergillus oryzae) that has been cultivated on rice or barley. Miso’s best-known usage is as the base of a soup that can be found on the menus of many Asian-themed restaurants in the U.S.

While many foods become more oxidized with time, fermented soy’s antioxidant capacity has been found to increase after eight to nine weeks, while lipid peroxidation levels remained low.1 Indeed, one can find miso on the market that has been aged from one to three years.

Miso Health Benefits

A review of bioactive peptides in soy enumerated their activities against oxidative stress, undesirable microbes, cancer, hypertension and immune dysfunction.2 A 2019 review of fermented soy products’ health benefits noted, “Several previous researches proved that soy products rich in protein can reduce the serum concentrations of total cholesterol, low-density lipoproteins (LDLs) and triglycerides if consumed instead of animal protein. Apart from these lipid-lowering effects, fermented soy products also proved to be effective in attenuating the effects of diabetes mellitus, blood pressure, cardiac disorders and cancer-related issues.”3

New research has found evidence of potential effects for fermented soy foods or miso against hepatitis A, hypertension, gastroesophageal reflux (GERD) and heart rate elevation in humans.4-8 In pre-clinical studies, miso appeared to be protective against stroke and visceral fat accumulation.9,10

Results from a meta-analysis of 330,826 participants in 23 studies, reported in the September 2019 issue of the Journal of the Academy of Nutrition and Dietetics, found that people who were among the highest consumers of soy had a 10% lower average risk of mortality during follow-up in comparison with subjects whose intake was among the lowest.11 A 10 milligram per day increase in soy isoflavones (which are contained in miso) was associated with a 7% decrease in the risk of dying from any cancer and a 9% lower risk of dying specifically from breast cancer. “Our findings may support the current recommendations to increase intake of soy for greater longevity,” S.M. Nachvak and colleagues concluded.

The fact that miso, despite its salt content, is associated with lower blood pressure is of interest. A study that examined the effects of soy foods on blood pressure among 4,165 Japanese men and women found no effects for non-fermented soy foods on the development of hypertension. However, subjects whose intake of fermented soy products (defined as miso and natto) was among the top one-third of participants had a 28% lower risk of developing high blood pressure than those whose intake was among the lowest third.6 A trial that compared the effects of consuming miso soup to a control soy food for eight weeks in participants with high-normal or stage 1 hypertension found that miso lowered nighttime blood pressure.5 In rats with salt-induced hypertension that were given miso, systolic blood pressure was reduced, which the researchers suggested was due to an increase in salt and water excretion.12

In an investigation that evaluated the effects of soy foods among 1,053 men and 373 women, total fermented soy food intake and miso intake in men were associated with a reduction in serum concentrations of interleukin-6 (IL-6), a marker of inflammation. “Some inflammatory biomarkers including [IL-6], IL-18 and C-reactive protein (CRP) have been shown to be associated with increased risk of type 2 diabetes, cardiovascular disease and many types of cancer,” Xiaolin Yang and colleagues explain. They note that “Fermented soy foods have been shown to contain greater amounts of polyamines including spermidine than the amounts in nonfermented soy products, and polyamines have been shown to be associated with cardioprotection and lifespan extension.”13

In human liver cells, miso inhibited replication of the hepatitis A virus (HAV) and increased the expression of a heat shock protein known as glucose-regulated protein 78 (GRP78), which had previously been shown to inhibit hepatitis A virus replication. Authors N. N. Win and colleagues concluded that “Japanese miso extracts can be used as effective dietary supplements for severe hepatitis A.”4

It was reported this year that the U.S. Food & Drug Administration (FDA) is considering revocation of approval of a permitted claim that diets low in saturated fat and cholesterol that include soy might reduce the risk of heart disease. However, the results of a meta-analysis of 43 of the 46 trials identified by the FDA that compared the effects of soy protein to non-soy protein on cholesterol levels concluded that at least 75% of the trials revealed a reduction in LDL cholesterol and that soy protein reduced LDL by an average of 3% to 4% in adults.14 Final action on the FDA proposal has been scheduled for December, 2019.

Benefits of Miso Soup When Sick

A study published last year that included 9,364 men and women enrolled in the ongoing Nagahama Study in Japan revealed a reduction in esophageal reflux and stomach upset in association with miso soup intake.7 Authors Fumika Mano and colleagues note that several amino acids contained in miso soup may promote gastric emptying.

But the most popular use of miso soup remains as a remedy for colds and flu. Although its benefits in seasonal illnesses have yet to be reported in published trials or studies, there have been a few investigations into its effects on immunity.15,16 In addition to the immune-balancing effects of soy peptides and isoflavones, miso contains the bacterium Tetragenococcus halophilus.17One strain of T. halophilus was recently found to have strong immunomodulatory effects that led the investigators to conclude that it has potential as a probiotic.17 So, when making miso soup, be sure to mix in the miso at the end of the process rather than boiling it in hot water or broth, to ensure that its beneficial bacteria remain viable.

Although chicken soup is the traditional Western go-to cold and flu remedy, miso may prove to be a worthy contender. Try it the next time you notice the malaise that can precede an illness. People have reported feeling better immediately.


  1. Tonolo F et al. Plant Foods Hum Nutr. 2019 Sep;74(3):287-292.
  2. Agyei D. Recent Pat Food Nutr Agric. 2015;7(2):100-7.
  3. Jayachandran M et al. Food Chem. 2019 Jan 15;271:362-371.
  4. Win NN et al. Int J Med Sci. 2018 Jul 30;15(11):1153-1159.
  5. Kondo H et al. Hypertens Res. 2019 Nov;42(11):1757-1767.
  6. Nozue M et al. J Nutr. 2017 Sep;147(9):1749-1756.
  7. Mano F et al. J Nutr Sci Vitaminol (Tokyo). 2018;64(5):367-373.
  8. Ito K et al. Intern Med. 2017;56(1):23-29.
  9. Watanabe H et al. Am J Hypertens. 2017 Dec 8;31(1):43-47.
  10. Okouchi R et al. Nutrients. 2019 Mar 6;11(3). pii: E560.
  11. Nachvak SM et al. J Acad Nutr Diet. 2019 Sep;119(9):1483-1500.
  12. Du DD et al. Clin Exp Hypertens. 2014;36(5):359-66.
  13. Yang X et al. J Med Invest. 2018;65(1.2):74-80.
  14. Blanco Mejia S et al. J Nutr. 2019 Jun 1;149(6):968-981.
  15. Yimit D et al. Nutrition. 2012 Feb;28(2):154-9.
  16. Zhang R et al. Nutr Cancer. 1997;29(1):24-8.
  17. Kumazawa T et al. PLoS One. 2018 Dec 26;13(12):e0208821.

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