Paleolithic Dieters: You May Have an Iodine Deficiency

A pinch of salt may cut the bitterness in a cup of coffee

An article in the European Journal of Clinical Nutrition suggests that paleolithic-type diets may be deficient in iodine. See my comment after the link below.

Abstract

BACKGROUND/OBJECTIVES:

Different diets are used for weight loss. A Paleolithic-type diet (PD) has beneficial metabolic effects, but two of the largest iodine sources, table salt and dairy products, are excluded. The objectives of this study were to compare 24-h urinary iodine concentration (24-UIC) in subjects on PD with 24-UIC in subjects on a diet according to the Nordic Nutrition Recommendations (NNR) and to study if PD results in a higher risk of developing iodine deficiency (ID), than NNR diet.

SUBJECTS/METHODS:

A 2-year prospective randomized trial in a tertiary referral center where healthy postmenopausal overweight or obese women were randomized to either PD (n=35) or NNR diet (n=35). Dietary iodine intake, 24-UIC, 24-h urinary iodine excretion (24-UIE), free thyroxin (FT4), free triiodothyronine (FT3) and thyrotropin (TSH) were measured at baseline, 6 and 24 months. Completeness of urine sampling was monitored by para-aminobenzoic acid and salt intake by urinary sodium.

RESULTS:

At baseline, median 24-UIC (71.0 μg/l) and 24-UIE (134.0 μg/d) were similar in the PD and NNR groups. After 6 months, 24-UIC had decreased to 36.0 μg/l (P=0.001) and 24-UIE to 77.0 μg/d (P=0.001) in the PD group; in the NNR group, levels were unaltered. FT4, TSH and FT3 were similar in both groups, except for FT3 at 6 months being lower in PD than in NNR group.

CONCLUSIONS:

A PD results in a higher risk of developing ID, than a diet according to the NNR. Therefore, we suggest iodine supplementation should be considered when on a PD.

(European Journal of Clinical Nutrition advance online publication, 13 September 2017; doi:10.1038/ejcn.2017.134.PMID: 28901333 DOI: 10.1038/ejcn.2017.134)

Source: A Paleolithic-type diet results in iodine deficiency: a 2-year randomized trial in postmenopausal obese women. – PubMed – NCBI

Parker here. I thought I knew a little about the Paleolithic diet, so was surprised to read above that table salt is excluded. It’s not excluded from the Paleobetic Diet. Most table salt purchased in the U.S. iodine-fortified. The introduction of iodized salt in the U.S. in 1924 raised IQ in iodine-deficient regions by 15 points!

Guyenet’s Response to Taubes’ “Sugar Is Killing Us” Hypothesis

An unregulated poison?

An unregulated poison?

Gary Taubes argues that sugar is the likely cause of the Western world’s epidemics of obesity, type 2 diabetes, had heart disease.

I agree it’s a strong contributor to those maladies, if only via it’s contribution to overweight and obesity. I wouldn’t say it’s the sole cause.

Here’s an excerpt from Guyenet’s response to Taubes to whet your appetite:

A Slow-Acting Toxin

According to Taubes, sugar may be a “toxin” and “the primary cause of diabetes, independent of its calories, and perhaps of obesity as well.” Elsewhere in the essay, coronary heart disease is added to the list. Yet Taubes asserts that this speculative hypothesis cannot currently be tested because there is so little existing research on sugar, and so little interest in conducting such research, that the research necessary to nail it down would take years to decades to complete and is not even on the radar screen of the funding agencies.

This belief is remarkable in light of the fact that a Google Scholar search returns hundreds of scientific papers on the health impacts of sugar, many of them human randomized controlled trials, and many funded by the U.S. National Institutes of Health. In reality, the health impacts of sugar are of considerable interest to the scientific community, and as such, they have been studied extensively. Having established that this research exists, let’s take a look at it.

The hypothesis that sugar is the primary cause of coronary heart disease is easily refuted. In the United States, coronary heart disease mortality has plummeted by more than 60 percent over the last half century, despite a 16 percent increase in added sugar intake. Roughly half of this decline can be attributed to better medical care, while the other half is attributed to underlying drivers of disease such as lower cholesterol and blood pressure levels and an impressive drop in cigarette use. This striking inverse relationship is incompatible with the hypothesis that sugar is the primary cause of coronary heart disease, although it doesn’t exonerate sugar.

Is sugar the primary cause of diabetes, “independent of its calories”? Research suggests that a high intake of refined sugar may increase diabetes risk, in large part via its ability to increase calorie intake and body fatness, but it is unlikely to be the primary cause. An immense amount of research, including several large multi-year randomized controlled trials, demonstrates beyond reasonable doubt that the primary causes of common (type 2) diabetes are excess body fat, insufficient physical activity, and genetic susceptibility factors.

The ultimate test of the hypothesis that sugar is the primary cause of obesity and diabetes would be to recruit a large number of people—perhaps even an entire country—and cut their sugar intake for a long time, ideally more than a decade. If the hypothesis is correct, rates of obesity and diabetes should start to decline, or at the very least stop increasing. Yet this experiment is far too ambitious to conduct.

Or is it? In fact, this experiment has already been conducted—in our very own country. Between 1999 and 2013, intake of added sugar declined by 18 percent, taking us back to our 1987 level of intake. Total carbohydrate intake declined as well. Over that same period of time, the prevalence of adult obesity surged from 31 percent to 38 percent, and the prevalence of diabetes also increased.

Source: Americans Eat Too Much Cake, but the Government Isn’t To Blame | Cato Unbound

Enjoy the view:

Well below room temp here

Not much sugar in this environment except for berries in spring and summer

Taubes partial response:

In stopping an epidemic, nothing is more important than correctly identifying its cause. Where we are today with obesity and diabetes reminds me of where infectious disease specialists were through most of the 19th century, when they blamed malaria and other insect-born diseases on miasma, or the bad air that came out of swamps. That was mildly effective, in that it was an explanation for why the rich in any particular town preferred to build their homes on hills, high above the miasma and, incidentally, away from the swamps and lowlands and slums where the vectors of these diseases were breeding. But only by identifying the vectors and the actual disease agents do we help everyone avoid them and eradicate the diseases. Only by unambiguously identifying the cause can we effectively design treatments to cure it. The kinds of explanations that Dr. Guyenet and Freedhoff put forth – highly palatable foods or ultra-processed foods – are the nutritional equivalents of the miasma explanation. They sound good; they might help some people incidentally eat the correct diets or offer a description of why other people already do, but they’re not the proximate cause of these epidemics. And there is a proximate cause. We have to find it. I can guarantee it’s not saturated fat, regardless of the effect of that nutrient on heart disease risk. What is it?

Now I am going to focus primarily on Dr. Guyenet’s response, as his was by far the most antagonistic, questioning both the history I present in the lead essay as well as the conclusions I’ve derived from the history and the science. While Dr. Guyenet does indeed challenge “specific and testable assertions” related to my lead essay, the one assertion he does manage to refute successfully is not, regrettably, an assertion I made in the article. As for the rest, the evidence against is not nearly as compelling as he presents it.

First, Dr. Guyenet examined “the 1980 Dietary Guidelines to determine if they condemn fat and take a weak stance on sugar as suggested.” He then set out to determine whether the 1980 Guidelines contributed to obesity, diabetes, and coronary heart disease. He concluded that they didn’t.

I was under the impression when I wrote the essay, though, and still am upon re-reading it, that I do not make such a simplistic assertion. The point that I made is not about the 1980 USDA Guidelines alone – Dr. Guyenet and I both note that they urged readers to avoid too much sugar – but rather the entire movement of the research community to demonize fat, and the journalistic coverage of it, and the series of government documents, and the consensus conferences that followed along because of it—all part of the same concerted public health effort that led us by the late 1980s to believe that the essence of a healthy diet is its relative absence of fat and saturated fat. As an unintended consequence, this ill-conceived dogma-building directed attention away from the possibility that sugar has deleterious effects independent of its calories.

These government reports, as I noted, included the FDA GRAS report on sugar in 1986, the Surgeon General’s Report on Nutrition and Health in 1988, the National Academy of Sciences Diet and Health report in 1989, the British COMA report on food policy the same year, and others. I could have also mentioned the 1984 NIH consensus conference on “lowering blood cholesterol to prevent heart disease” that followed on this legendary Time Magazine cover – “Cholesterol, And Now the Bad News” – and the founding in 1986 of the National Cholesterol Education Program, which published its guidelines for cholesterol lowering the following year. All focused on dietary fat and serum cholesterol as the agents of heart disease and all mostly or completely ignored the evolving science on insulin resistance and metabolic syndrome that implicated sugar and other processed carbohydrates.

Indeed, if anything, the more relevant of the two USDA Dietary Guidelines, the one that Dr. Guyenet does not address, is the 1985 version that declared without a caveat, as I noted, that “too much sugar in your diet does not cause diabetes.” This is, of course, remains the critical question and the one that yet has to be rigorously tested (ignoring the tautology implied by the use of the words “too much”).

Dr. Guyenet, Dr. Freedhoff, and I all agree that had Americans eaten as the guidelines cautioned (and just as Michael Pollan would have preferred as well), we’d all very likely be healthier. But we didn’t. The question is whether the dietary fat/serum cholesterol/heart disease obsession directed attention away from the hypothesis that sugar causes heart disease, diabetes, and perhaps obesity as well through its effect on insulin resistance. The secondary question is whether this obsession in government documents, programs, journalistic coverage, and (pseudo)scientific reviews explains why we continued to eat such high sugar diets. As Dr. Guyenet notes, Americans still consume a significant amount of our calories from grain-based desserts and sugary beverages. But why? By focusing on the straw man of the 1980 guidelines, Dr. Guyenet fails to address that question. That he’s taking on a straw man makes me thinks he’s more interested in appearing to win an argument than in dealing with what may be the single most important public health issue of our era.

A key point to make, as Professor Kealey does, is that Americans did indeed respond to the dietary dogma of the 1970s and 1980s by changing their diets. Dr. Freedhoff and Dr. Guyenet are wrong in this regard when they attend only to the total percentage and amounts of fats, carbohydrates, and protein in our diets, and not the type of fats, carbohydrates, and even protein. Looking at what we ate instead of how much we ate supports the supposition that Americans heard the advice on fat and acted on it, even as we were ignoring the sugar advice. As the USDA reports, between 1970 and 2005, we cut down on our use of butter (-17%) and lard (-66%), while almost doubling vegetable oil consumption (from 38.5 pounds per capita yearly to 73.7); we more than doubled how much chicken we ate (33.8 pounds per capita yearly to 73.6, probably skinless white meat, but I’m speculating), while reducing our red meat consumption by 17 percent, and beef by 22 percent. We cut back on eggs, too. So while total fat consumption decreased only marginally, as Drs. Freedhoff and Guyenet note, that marginal decrease is accompanied by a reduction in animal fats and their replacement by vegetable oils, which were thought to be heart healthy and still are (perhaps also erroneously). The type of fats we consumed and the type of foods we consumed changed significantly, and this change was very much in accord with what we were being told.

The post-1980 focus on dietary fat also led to the creation and sale of thousands, perhaps tens of thousands, of non-fat and low-fat food-like substances (credit for the terminology once again to Mr. Pollan). In this instance, the CDC’s publication Healthy People 2000 is informative: Healthy People 2000 included multiple “nutrition objectives” aimed at reducing dietary fat consumption, including the creation of 5,000 low-fat or low-saturated fat products. It included nutrition objectives to reduce salt intake and increase complex carbohydrate and fiber consumption, but included no such objective for sugar or sugar-rich foods. Why not? Indeed, I find that the words “sugar” or “sugars” appear only five times in the almost 400-page final review of how well the guidelines were met. In 1995, the American Heart Association counseled in one of its pamphlets that Americans could control the amount and kind of fat consumed by “choos[ing] snacks from other food groups such as…..low-fat cookies, low-fat crackers,…unsalted pretzels, hard candy, gum drops, sugar, syrup, honey, jam, jelly, marmalade (as spreads).” In 2000, the AHA published this cookbook of low-fat and luscious sugar-rich “soul-satisfying” desserts. I don’t know if Dr. Guyenet would describe this as a “weak stand” on sugar or not, but it does shed light on our failure to limit sugar consumption during a period in which all public health advice was focused on reducing fat.

The more important question, and a very different one, is whether our sugar consumption has uniquely deleterious effects on our health. To refute the claim that consuming sugar might cause heart disease, Dr. Guyenet points out that heart disease mortality has dropped precipitously over the years of the obesity and diabetes epidemics and during a period when sugar consumption clearly increased (technically “caloric sweeteners” since the increase was due primarily to high-fructose corn syrup). Professor Kealey makes a similar point but with a far more nuanced perspective about how mortality rates are confounded by what are, after all, a half-century’s worth of very concerted efforts by medical researchers, the pharmaceutical and medical industry, and public health authorities to reduce mortality. That these efforts succeeded in reducing mortality is indeed commendable, but it makes it far more difficult than Dr. Guyenet suggests to derive meaning from the mortality data. If it’s evidence against the sugar hypothesis, it’s very weak evidence.

Dr. Michael Eades weighs in with words of wisdom.

Is Your Blood Glucose Meter Accurate? 

DiaTribe has an article on glucose meter accuracy by Jeemin Kwon and Adam Brown. I quote:

Results from the Diabetes Technology Society’s Blood Glucose Meter Surveillance Program identifies only six out of 18 meters that passed. Did yours make the cut?

The Diabetes Technology Society (DTS) recently revealed long-awaited results from its Blood Glucose Monitor System (BGMS) Surveillance Program. The rigorous study tested the accuracy of 18 popular blood glucose meters (BGM) used in the US. These FDA-cleared meters were purchased through retail outlets and tested rigorously at three study sites in over 1,000 people (including 840 people with diabetes). The results were troubling: only six out of the 18 devices met the DTS passing standard for meter accuracy – within 15% or 15 mg/dl of the laboratory value in over 95% of trials.

The devices that passed were:

  • Contour Next from Ascensia (formerly Bayer) – 100%
  • Accu-Chek Aviva Plus from Roche – 98%
  • Walmart ReliOn Confirm (Micro) from Arkray – 97%
  • CVS Advanced from Agamatrix – 97%
  • FreeStyle Lite from Abbott – 96%
  • Accu-Chek SmartView from Roche – 95%

The devices that failed were:  

  • Walmart ReliOn Prime from Arkray – 92%
  • OneTouch Verio from LifeScan – 92%
  • Prodigy Auto Code from Prodigy – 90%
  • OneTouch Ultra 2 from LifeScan – 90%
  • Walmart ReliOn Ultima from Abbott – 89%
  • Contour Classic from Bayer – 89%
  • Embrace from Omnis Health – 88%
  • True Result from HDI/Nipro – 88%
  • True Track from HDI/Nipro – 81%
  • Solus V2 from BioSense Medical – 76%
  • Advocate Redi-Code+ from Diabetic Supply of Suncoast – 76%
  • Gmate Smart from Philosys – 71%

Source: Are Blood Glucose Meters Accurate? New Data on 18 Meters | diaTribe

Natural Ways to Treat Hypertension

You may need to cut back on alcohol Photo copyright: Steve Parker MD

You may need to cut back on alcohol.
Photo copyright: Steve Parker

Drugs to control hypertension can save your life. I prescribe them all the time. However, there are also “natural” ways to control high blood pressure. Click the link at bottom for some of the better known methods from Kerri-Ann Jennings, RD. If you’re trying to avoid drugs, you’ll probably need a combination of tricks. And they don’t work for everybody.

Even if you’re already on drugs, you may be able to cut back or stop them if you adopt some of these tips.

“High blood pressure is a dangerous condition that can damage your heart. It affects one in three people in the US and 1 billion people worldwide.

If left uncontrolled, it raises your risk of heart disease and stroke.

But there’s good news. There are a number of things you can do to lower your blood pressure naturally, even without medication.Here are 15 natural ways to combat high blood pressure.”

Source: 15 Natural Ways to Lower Your Blood Pressure

h/t Jan at The Low Carb Diabetic

Butchered Bones Found in Canada Indicate Humans Came to North America 24,000 Years Ago

Fresh off the Bering Strait from Siberia?

Fresh off the Bering Strait from Siberia?

From Ancient Origins:

“Archaeologists have found a set of butchered bones dating back 24,000 years in Bluefish Caves, Yukon, Canada, which are the oldest signs of human habitation ever discovered in North America. Until recently, it was believed that the culture that represented the continent’s first inhabitants was the Clovis culture. However, the discovery of the butchered bones challenges that theory, providing evidence that human occupation preceded the arrival of the Clovis people by as much as 10,000 years.

For decades, it has been believed that the first Americans crossed the Bering Strait from Siberia about 14,000 years ago and quickly colonized North America.”

Source: 24,000-Year-Old Butchered Bones Found in Canada Change Known History of North America | Ancient Origins

Does Cold Exposure Help With Weight Loss?

Well below room temp here

Probably well below room temp here

David Mendosa found a 2016 research report suggesting that cool temperatures may help with weight management by activating our brown fat, which burns more calories. Heat generated by brown fat is derived from glucose and triglycerides. Keep in mind as you read further that a comfortable environment temperature for a clothed human is about 23°C or 73°F. Those temps don’t stress our bodies by requiring us to either generate or dissipate extra body heat.

David writes:

Researchers have discovered that when we get mildly cold, which they define as being cool without shivering, our bodies burn more calories. As a result, managing our weight can be easier.
This is the conclusion of a recent review that two researchers at Maastricht University Medical Center in the Netherlands published in the November 2016 issue of the professional journal Diabetologia. The title of their article, “Combatting type 2 diabetes by turning up the heat,” puzzled me at first.

The title confused me because the study is about turning down the heat in the room we’re in. But then our bodies compensate by turning up their internal heat production.

When our body does this, its energy expenditure increases, ratcheting up our metabolism. Being mildly cold revs up our bodies’ brown fat, which unlike white fat, burns calories instead of storing them.

It’s not quite clear how much cold exposure it takes to turn on your brown fat. From the link above:

Cold acclimation by intermittent exposure to a cool (14–17°C) [57–63°F], or cold (10°C) [50°F] environment resulted in significant increases in NST [non-shivering thermogenesis or heat production] capacity. A 10 day cold acclimation study with 6 hour exposure to 14–15°C [57–59°F] per day was enough to significantly increase NST by 65% on average. A 6 week mild cold acclimation study (daily 2 hour cold exposure at 17°C [63°F]) also resulted in an increase in NST together with a concomitant decrease in body fat mass. The latter two studies also revealed significant increases in BAT [brown adipose tissue] presence and activation. All in all, cold-induced BAT activity is significant in adults and parallels NST. The actual quantitative contributions of BAT and of other tissues (e.g. skeletal muscle) to whole-body NST are, however, not elucidated and await further studies. Furthermore, more information is needed on the duration, timing and temperatures to find out which treatments are most effective with respect to increasing NST.

Furthermore, cold exposure over the course of 10 days increased insulin sensitivity in T2 diabetics by 43%. Eight study subjects, probably in the Netherlands, were exposed to temps of 14–15°C [57–59°F] but I don’t know for how many hours a day. Increased insulin sensitivity should help keep a lid on blood sugar levels and reduce the need for diabetes drugs.

In case you’re elderly, obese, or have type 2 diabetes, be aware that the activation of brown fat by cold exposure is not as robust as in others.

On the other hand, I found evidence that higher ambient temperatures (above 23°C) [73°F] may also help with weight management, regardless of what brown fat is doing. Science is hard.

Steve Parker, M.D.

PS: Check out my books for more ideas on weight management.

 

Paleo Diet Reduced Low-Grade Inflammation In Obese Postmenopausal Women

I haven’t read the entire article, so probably can’t answer any of your questions. When you read “android fat” below, think “belly fat,” which is linked to poor health outcomes compared to non-belly fat.

OBJECTIVE: Abdominal fat accumulation after menopause is associated with low-grade inflammation and increased risk of metabolic disorders. Effective long-term lifestyle treatment is therefore needed.

METHODS: Seventy healthy postmenopausal women (age 60 ± 5.6 years) with BMI 32.5 ± 5.5 were randomized to a Paleolithic-type diet (PD) or a prudent control diet (CD) for 24 months. Blood samples and fat biopsies were collected at baseline, 6 months, and 24 months to analyze inflammation-related parameters.

RESULTS: Android fat decreased significantly more in the PD group (P = 0.009) during the first 6 months with weight maintenance at 24 months in both groups. Long-term significant effects (P < 0.001) on adipose gene expression were found for toll-like receptor 4 (decreased at 24 months) and macrophage migration inhibitory factor (increased at 24 months) in both groups. Serum interleukin 6 (IL-6) and tumor necrosis factor α levels were decreased at 24 months in both groups (P < 0.001) with a significant diet-by-time interaction for serum IL-6 (P = 0.022). High-sensitivity C-reactive protein was decreased in the PD group at 24 months (P = 0.001).

CONCLUSIONS: A reduction of abdominal obesity in postmenopausal women is linked to specific changes in inflammation-related adipose gene expression.

Source: Attenuated Low-Grade Inflammation Following Long-Term Dietary Intervention in Postmenopausal Women with Obesity. – PubMed – NCBI

Have You Considered the Lowly Rutabaga?

Jan over at The Low Carb Diabetic is getting me motivated to try a new vegetable: rutabaga.

Click the link below for Jan’s post and more photos and recipes.

“The picture above shows what Americans know as “rutabaga”. The Scottish call it “neeps” and serve it with haggis. I know it as swede, a fairly recent root vegetable, which is thought to have originated around the 17th century in Bohemia. In 1620 a Swiss botanist described the root vegetable, believed to be a hybrid of the cabbage and the turnip. By 1664 it was growing in England. A good source of vitamin.C, fibre, folate and potassium. It’s low in calories.”

Source: The Low Carb Diabetic: Swede / Rutabaga : How will you serve this low carb vegetable

Do you like rutabagas?

PS: If the copyright owner of the rutabaga photo wants me to take it down, contact Steve Parker, M.D., and it shall be done posthaste.

From 2012: Largest Healthcare Fraud Settlement In History Involves T2 Diabetes Drug Avandia

Your friendly neighborhood drug supplier

Your friendly neighborhood drug supplier

This will help you understand why I favor diet modification over drug therapy for type 2 diabetes:

“Global health care giant GlaxoSmithKline LLC (GSK) agreed to plead guilty and to pay $3 billion to resolve its criminal and civil liability arising from the company’s unlawful promotion of certain prescription drugs, its failure to report certain safety data, and its civil liability for alleged false price reporting practices, the Justice Department announced today. The resolution is the largest health care fraud settlement in U.S. history and the largest payment ever by a drug company. GSK agreed to plead guilty to a three-count criminal information, including two counts of introducing misbranded drugs, Paxil and Wellbutrin, into interstate commerce and one count of failing to report safety data about the drug Avandia to the Food and Drug Administration (FDA). Under the terms of the plea agreement, GSK will pay a total of $1 billion, including a criminal fine of $956,814,400 and forfeiture in the amount of $43,185,600. The criminal plea agreement also includes certain non-monetary compliance commitments and certifications by GSK’s U.S. president and board of directors. GSK’s guilty plea and sentence is not final until accepted by the U.S. District Court. GSK will also pay $2 billion to resolve its civil liabilities with the federal government under the False Claims Act, as well as the states. The civil settlement resolves claims relating to Paxil, Wellbutrin and Avandia, as well as additional drugs, and also resolves pricing fraud allegations.”

Source: GlaxoSmithKline to Plead Guilty and Pay $3 Billion to Resolve Fraud Allegations and Failure to Report Safety Data | OPA | Department of Justice

Regarding Avandia:

“The United States alleges that, between 2001 and 2007, GSK failed to include certain safety data about Avandia, a diabetes drug, in reports to the FDA that are meant to allow the FDA to determine if a drug continues to be safe for its approved indications and to spot drug safety trends. The missing information included data regarding certain post-marketing studies, as well as data regarding two studies undertaken in response to European regulators’ concerns about the cardiovascular safety of Avandia. Since 2007, the FDA has added two black box warnings to the Avandia label to alert physicians about the potential increased risk of (1) congestive heart failure, and (2) myocardial infarction (heart attack). GSK has agreed to plead guilty to failing to report data to the FDA and has agreed to pay a criminal fine in the amount of $242,612,800 for its unlawful conduct concerning Avandia.”

And…

“In its civil settlement agreement, the United States alleges that GSK promoted Avandia to physicians and other health care providers with false and misleading representations about Avandia’s safety profile, causing false claims to be submitted to federal health care programs. Specifically, the United States alleges that GSK stated that Avandia had a positive cholesterol profile despite having no well-controlled studies to support that message. The United States also alleges that the company sponsored programs suggesting cardiovascular benefits from Avandia therapy despite warnings on the FDA-approved label regarding cardiovascular risks. GSK has agreed to pay $657 million relating to false claims arising from misrepresentations about Avandia. The federal share of this settlement is $508 million and the state share is $149 million.”

 

Regain Muscle Mass Even If Over 60

She'll lose muscle fibers if she gets too sedentary as she ages

She’ll lose muscle if she gets too sedentary as she ages

“Our lab and others have shown repeatedly” that older muscles will grow and strengthen, says Marcas Bamman, a professor of integrative biology at the University of Alabama at Birmingham. In his studies, men and women in their 60s and 70s who began supervised weight training developed muscles that were as large and strong as those of your average 40-year-old.”

Source: Can You Regain Muscle Mass After Age 60? – The New York Times

Dr. Bamman says older folks (over 60?) don’t add new muscle fibers like young’uns do. But an effective exercise program will cause hypertrophy (growth) of the existing muscle fibers. “Effectiveness” probably depend on exhausting muscle groups during weight training.