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The keto diet helps men – not women – lose weight, new research suggests
One group of women still seem to benefit from the popular diet.
- Medical professionals and dieters have long noticed differences in the efficacy of the keto diet between the sexes.
- A new study suggests that estrogen plays a role in preventing women from losing weight on the keto diet.
- More research is needed before scientists know exactly how the keto diet's effects vary between the sexes.
It's long been observed that men seem to have an easier time than women in terms of losing weight on the keto diet. The results of a new study on the keto diet's effects on mice support that anecdotal claim, suggesting that sexual hormones might prevent the high-fat diet from helping females lose weight.
At the annual meeting of the Endocrine Society on Sunday, researchers from the University of Iowa discussed a soon-to-be-published study showing how female mice on the keto diet were less likely than males to lose weight, and more likely to experienced impaired blood sugar control.
In the experiments, researchers put a group of mice on the keto diet or a regular diet, which served as the control.
- Keto diet: 75 percent fat, 3 percent carbs, 8 percent protein
- Regular diet: 7 percent fat, 47 percent carbs, 19 percent protein
After 15 weeks on the keto diet, the male mice experienced losses of body weight and body fat, while the female group actually gained weight. The researchers speculated that estrogen might be interfering with the weight-loss process, so they removed ovaries from some of the mice. This caused females to start experiencing the same weight-loss effects observed in the male group.
"Our studies suggest that sex hormones might modulate the way that male versus female mice respond to ketogenic diets," lead investigator Jesse Cochran, a research assistant at the University of Iowa, told Inverse.
The male mice experienced another, less desirable change: Their livers showed stronger signs of fibrosis — the thickening and scarring of connective tissue — and fatty storage than the female mice. The males had higher levels of a hormone called FG21, which previous studies have shown is released in response to liver damage.
Is the keto diet bad for the liver?
The intuitive answer might be yes, considering the keto diet calls for eating lots of fats, and having too much fat (particularly triglycerides) in your liver can lead to inflammation and cell death. However, some research suggests that a responsibly implemented keto diet can actually improve liver health.
For example, a 2018 study tracked the effects of the keto diet on 10 mildly obese people with fatty livers. Ann Fernholm, science journalist and founder of the not-for-profit Dietary Science Foundation, said the study offered an "extremely detailed map showing what happens when a person cuts down on sugar and starch in their diet.
"The liver metabolism changed almost immediately," she wrote for Diet Doctor. "Instead of creating fat, it started burning it and already in the first day you could see a significant reduction in liver fat. As a great side effect, the participants also improved their cholesterol profiles. The microbiome also changed. A surprising discovery was that it started producing more folic acid, a vitamin which is important in the liver's metabolism. Low levels of folic acid has earlier been associated with an increased risk of fatty liver."
Still, more research is needed
Despite its popularity, there's still much scientists don't know about the keto diet, and most medical professionals stop short of recommending the diet unless it's prescribed to epileptics.
"The keto diet is primarily used to help reduce the frequency of epileptic seizures in children," said registered dietitian Kathy McManus, director of the Department of Nutrition at Harvard-affiliated Brigham and Women's Hospital. "While it also has been tried for weight loss, only short-term results have been studied, and the results have been mixed. We don't know if it works in the long term, nor whether it's safe."
The mixed results on keto diet studies could be explained, in part, by discrepancies in efficacy between the sexes, and a lack of solid research on how females respond to the diet.
"Most studies of the ketogenic diet for weight loss have taken place in small numbers of patients or in only male mice, so sex-based differences in response to this diet are unclear," said senior investigator E. Dale Abel, M.D., Ph.D., chair of the University of Iowa Department of Internal Medicine and president-elect of the Endocrine Society.
Regarding the recent research, it remains unclear whether similar studies conducted with human participants would yield the same results.
Can the keto diet work for some women?
Interestingly, the recent study suggests it can.
"[The finding that ovariectomized mice experienced weight loss] suggests that postmenopausal women could potentially experience better weight loss outcomes with the ketogenic diet compared to younger women," Cochran said.
This seems to match the observations of some medical professionals prior to the recent research.
"My anecdotal observation in my medical office and working with people online is that men perform better in nutritional ketosis compared with women, particularly women aged 40 and older," wrote Sara Gottfried, a board-certified gynecologist, on her website. "My female patients, myself included, have more problems on keto with their stress hormones (i.e. producing too much cortisol), thyroid function, and may develop menstrual irregularities. At the root of these problems is dysfunction of the control system for hormones, the hypothalamic-pituitary-adrenal-thyroid-gonadal (HPATG) axis."
Since the initial use of ketogenic diets (KD) as adjunctive treatment for epilepsy, these diets are being increasingly used to promote weight loss and to reduce the risk of metabolic sequelae of severe obesity. Typical KD are very low in carbohydrate and high in fat, promoting hepatic production of ketone bodies. Most animal studies tend to be performed in male mice, and few studies have evaluated gender differences in response to KD. To explore sex differences in response to KD, female and male wild-type mice on the C57BL/6J background were fed either a control diet (CD- 7% fat, 47% carb., 19% protein) or KD (75% fat, 3% carb., 8% protein), following weaning. Females on the CD manifested higher levels of circulating β-hydroxybutyrate (β-HB) than males (2.86-fold, p<0.05). Circulating β-HB concentrations increased with KD in males and females (1.30-fold & 5.05-fold, p<10-4& p<0.01 respectively) with higher concentrations in females. After 15 weeks of feeding, females on KD displayed an increase in body weight (1.07-fold KD vs. CD, p<0.05) while body weight declined in males (0.88-fold, p<0.05). Nuclear magnetic resonance (NMR) analysis revealed elevated lean mass in 18-week old females (1.07-fold, p<0.05), but a significant reduction in fat mass in males (0.49-fold, p<0.05) relative to sex-matched mice on CD. The female mice on KD developed impaired glucose tolerance with a 1.35-fold increase in glucose tolerance test area under the curve (GTT AUC) (p<0.001) relative to CD females. In contrast, fasting glucose levels were lower in males on KD (131.8 ± 12.5 mg/ dl vs. 169.2 ± 6.3 mg/dl, p<0.05). Despite no significant change in GTT AUC, the male mice on KD displayed elevated blood glucose concentrations 30 minutes after injection relative to males on CD (344.9 ± 18.7 mg/ dl vs. 272.0 ± 10.31 mg/dl, p<0.05). However, after 120 minutes, blood glucose levels returned to initial levels. To further investigate the role of estrogen in this sexual dimorphism, female mice were ovariectomized (OVX) and randomized to receive either a CD or KD after weaning. At 15 weeks old, OVX mice on KD displayed decreased body weight (0.84-fold, p<0.0001) and fat mass (0.65-fold, p<0.001) relative to CD-fed mice. Despite changes in body composition, OVX mice on KD still exhibited impaired glucose tolerance with a 1.4-fold increase in GTT AUC comparable to OVX mice on CD (p<0.05). In conclusion, significant sex differences exist in terms of body composition and metabolism in response to ketogenic diet, which may partially be attributed to estrogen.
Innovation in manufacturing has crawled since the 1950s. That's about to speed up.
Health officials in China reported that a man was infected with bubonic plague, the infectious disease that caused the Black Death.
- The case was reported in the city of Bayannur, which has issued a level-three plague prevention warning.
- Modern antibiotics can effectively treat bubonic plague, which spreads mainly by fleas.
- Chinese health officials are also monitoring a newly discovered type of swine flu that has the potential to develop into a pandemic virus.
Bacteria under microscope
needpix.com<p>Today, bubonic plague can be treated effectively with antibiotics.</p><p style="margin-left: 20px;">"Unlike in the 14th century, we now have an understanding of how this disease is transmitted," Dr. Shanthi Kappagoda, an infectious disease physician at Stanford Health Care, told <a href="https://www.healthline.com/health-news/seriously-dont-worry-about-the-plague#Heres-how-the-plague-spreads" target="_blank">Healthline</a>. "We know how to prevent it — avoid handling sick or dead animals in areas where there is transmission. We are also able to treat patients who are infected with effective antibiotics, and can give antibiotics to people who may have been exposed to the bacteria [and] prevent them [from] getting sick."</p>
This plague patient is displaying a swollen, ruptured inguinal lymph node, or buboe.
Centers for Disease Control and Prevention<p>Still, hundreds of people develop bubonic plague every year. In the U.S., a handful of cases occur annually, particularly in New Mexico, Arizona and Colorado, <a href="https://www.cdc.gov/plague/faq/index.html" target="_blank">where habitats allow the bacteria to spread more easily among wild rodent populations</a>. But these cases are very rare, mainly because you need to be in close contact with rodents in order to get infected. And though plague can spread from human to human, this <a href="https://www.healthline.com/health-news/seriously-dont-worry-about-the-plague#Heres-how-the-plague-spreads" target="_blank">only occurs with pneumonic plague</a>, and transmission is also rare.</p>
A new swine flu in China<p>Last week, researchers in China also reported another public health concern: a new virus that has "all the essential hallmarks" of a pandemic virus.<br></p><p>In a paper published in the <a href="https://www.pnas.org/content/early/2020/06/23/1921186117" target="_blank">Proceedings of the National Academy of Sciences</a>, researchers say the virus was discovered in pigs in China, and it descended from the H1N1 virus, commonly called "swine flu." That virus was able to transmit from human to human, and it killed an estimated 151,700 to 575,400 people worldwide from 2009 to 2010, according to the Centers for Disease Control and Prevention.</p>There's no evidence showing that the new virus can spread from person to person. But the researchers did find that 10 percent of swine workers had been infected by the virus, called G4 reassortant EA H1N1. This level of infectivity raises concerns, because it "greatly enhances the opportunity for virus adaptation in humans and raises concerns for the possible generation of pandemic viruses," the researchers wrote.
So far, 30 student teams have entered the Indy Autonomous Challenge, scheduled for October 2021.
- The Indy Autonomous Challenge will task student teams with developing self-driving software for race cars.
- The competition requires cars to complete 20 laps within 25 minutes, meaning cars would need to average about 110 mph.
- The organizers say they hope to advance the field of driverless cars and "inspire the next generation of STEM talent."
Indy Autonomous Challenge<p>Completing the race in 25 minutes means the cars will need to average about 110 miles per hour. So, while the race may end up being a bit slower than a typical Indy 500 competition, in which winners average speeds of over 160 mph, it's still set to be the fastest autonomous race featuring full-size cars.</p><p style="margin-left: 20px;">"There is no human redundancy there," Matt Peak, managing director for Energy Systems Network, a nonprofit that develops technology for the automation and energy sectors, told the <a href="https://www.post-gazette.com/business/tech-news/2020/06/01/Indy-Autonomous-Challenge-Indy-500-Indianapolis-Motor-Speedway-Ansys-Aptiv-self-driving-cars/stories/202005280137" target="_blank">Pittsburgh Post-Gazette</a>. "Either your car makes this happen or smash into the wall you go."</p>
Illustration of the Indy Autonomous Challenge
Indy Autonomous Challenge<p>The Indy Autonomous Challenge <a href="https://www.indyautonomouschallenge.com/rules" target="_blank">describes</a> itself as a "past-the-post" competition, which "refers to a binary, objective, measurable performance rather than a subjective evaluation, judgement, or recognition."</p><p>This competition design was inspired by the 2004 DARPA Grand Challenge, which tasked teams with developing driverless cars and sending them along a 150-mile route in Southern California for a chance to win $1 million. But that prize went unclaimed, because within a few hours after starting, all the vehicles had suffered some kind of critical failure.</p>
Indianapolis Motor Speedway
Indy Autonomous Challenge<p>One factor that could prevent a similar outcome in the upcoming race is the ability to test-run cars on a virtual racetrack. The simulation software company Ansys Inc. has already developed a model of the Indianapolis Motor Speedway on which teams will test their algorithms as part of a series of qualifying rounds.</p><p style="margin-left: 20px;">"We can create, with physics, multiple real-life scenarios that are reflective of the real world," Ansys President Ajei Gopal told <a href="https://www.wsj.com/articles/autonomous-vehicles-to-race-at-indianapolis-motor-speedway-11595237401?mod=e2tw" target="_blank">The Wall Street Journal</a>. "We can use that to train the AI, so it starts to come up to speed."</p><p>Still, the race could reveal that self-driving cars aren't quite ready to race at speeds of over 110 mph. After all, regular self-driving cars already face enough logistical and technical roadblocks, including <a href="https://www.bbc.com/news/technology-53349313#:~:text=Tesla%20will%20be%20able%20to,no%20driver%20input%2C%20he%20said." target="_blank">crumbling infrastructure, communication issues</a> and the <a href="https://bigthink.com/paul-ratner/would-you-ride-in-a-car-thats-programmed-to-kill-you" target="_self">fateful moral decisions driverless cars will have to make in split seconds</a>.</p>But the Indy Autonomous Challenge <a href="https://static1.squarespace.com/static/5da73021d0636f4ec706fa0a/t/5dc0680c41954d4ef41ec2b2/1572890638793/Indy+Autonomous+Challenge+Ruleset+-+v5NOV2019+%282%29.pdf" target="_blank">says</a> its main goal is to advance the industry, by challenging "students around the world to imagine, invent, and prove a new generation of automated vehicle (AV) software and inspire the next generation of STEM talent."
A new Harvard study finds that the language you use affects patient outcome.
- A study at Harvard's McLean Hospital claims that using the language of chemical imbalances worsens patient outcomes.
- Though psychiatry has largely abandoned DSM categories, professor Joseph E Davis writes that the field continues to strive for a "brain-based diagnostic system."
- Chemical explanations of mental health appear to benefit pharmaceutical companies far more than patients.
Challenging the Chemical Imbalance Theory of Mental Disorders: Robert Whitaker, Journalist<span style="display:block;position:relative;padding-top:56.25%;" class="rm-shortcode" data-rm-shortcode-id="41699c8c2cb2aee9271a36646e0bee7d"><iframe type="lazy-iframe" data-runner-src="https://www.youtube.com/embed/-8BDC7i8Yyw?rel=0" width="100%" height="auto" frameborder="0" scrolling="no" style="position:absolute;top:0;left:0;width:100%;height:100%;"></iframe></span><p>This is a far cry from Howard Rusk's 1947 NY Times editorial calling for mental healt</p><p>h disorders to be treated similarly to physical disease (such as diabetes and cancer). This mindset—not attributable to Rusk alone; he was merely relaying the psychiatric currency of the time—has dominated the field for decades: mental anguish is a genetic and/or chemical-deficiency disorder that must be treated pharmacologically.</p><p>Even as psychiatry untethered from DSM categories, the field still used chemistry to validate its existence. Psychotherapy, arguably the most efficient means for managing much of our anxiety and depression, is time- and labor-intensive. Counseling requires an empathetic and wizened ear to guide the patient to do the work. Ingesting a pill to do that work for you is more seductive, and easier. As Davis writes, even though the industry abandoned the DSM, it continues to strive for a "brain-based diagnostic system." </p><p>That language has infiltrated public consciousness. The team at McLean surveyed 279 patients seeking acute treatment for depression. As they note, the causes of psychological distress have constantly shifted over the millennia: humoral imbalance in the ancient world; spiritual possession in medieval times; early childhood experiences around the time of Freud; maladaptive thought patterns dominant in the latter half of last century. While the team found that psychosocial explanations remain popular, biogenetic explanations (such as the chemical imbalance theory) are becoming more prominent. </p><p>Interestingly, the 80 people Davis interviewed for his book predominantly relied on biogenetic explanations. Instead of doctors diagnosing patients, as you might expect, they increasingly serve to confirm what patients come in suspecting. Patients arrive at medical offices confident in their self-diagnoses. They believe a pill is the best course of treatment, largely because they saw an advertisement or listened to a friend. Doctors too often oblige without further curiosity as to the reasons for their distress. </p>
Image: Illustration Forest / Shutterstock<p>While medicalizing mental health softens the stigma of depression—if a disorder is inheritable, it was never really your fault—it also disempowers the patient. The team at McLean writes,</p><p style="margin-left: 20px;">"More recent studies indicate that participants who are told that their depression is caused by a chemical imbalance or genetic abnormality expect to have depression for a longer period, report more depressive symptoms, and feel they have less control over their negative emotions."</p><p>Davis points out the language used by direct-to-consumer advertising prevalent in America. Doctors, media, and advertising agencies converge around common messages, such as everyday blues is a "real medical condition," everyone is susceptible to clinical depression, and drugs correct underlying somatic conditions that you never consciously control. He continues,</p><p style="margin-left: 20px;">"Your inner life and evaluative stance are of marginal, if any, relevance; counseling or psychotherapy aimed at self-insight would serve little purpose." </p><p>The McLean team discovered a similar phenomenon: patients expect little from psychotherapy and a lot from pills. When depression is treated as the result of an internal and immutable essence instead of environmental conditions, behavioral changes are not expected to make much difference. Chemistry rules the popular imagination.</p>