Last year more than 1.7 million people were diagnosed with cancer in the United States. Cancer can be difficult to treat because each tumor is unique. Scientists are now gaining a better understanding of the changes that lead to cancer—and figuring out how to target them for personalized treatments.
“Cancer treatment is changing at a very fast pace,” says Dr. Patricia M. LoRusso, an NIH-funded cancer treatment expert at Yale Cancer Center. “What somebody got a year ago may not necessarily be the same treatment recommended for another person today.”
For decades, doctors have treated cancers based on where a tumor first started, such as in the lung or colon. But often, a treatment that works well for one person doesn’t work as well for another.
Research has revealed that each tumor has a unique combination of genetic changes. Cancer is caused by changes in genes that control the ways cells grow and survive. The cells begin to divide without stopping. They form growths called tumors, and some spread to other parts of the body.
The genetic changes that cause cancer are most often from exposure to sunlight, tobacco, and other things in the environment that can damage genes. But some cancer-causing genes can also be passed down from your parents.
These insights have led scientists to look for the unique genetic features of each person’s tumor and then attack those specifically.
“Many times, we’re trying to turn off certain pathways in the tumor that are activated and that cause it to continue to grow,” LoRusso says. This type of treatment is called “targeted therapy” because the drugs target the specific changes in cancer cells that help them to survive and spread.
Doctors can now send a sample of the tumor to a lab to identify important genetic changes. The doctor can then match the unique changes with the treatment that is most likely to help.
“There are several drugs that are now on the market that have made a huge impact in the treatment of several types of cancer,” LoRusso says.
Genetic testing isn’t available yet for many types of cancer. NIH-funded studies are looking for ways to develop targeted therapies for more cancer types.
Another approach researchers are taking is to use a patient’s own disease-fighting cells, called immune cells, to find and kill cancer cells in their body. Scientists have successfully inserted cancer-fighting genes into a patient’s immune cells. Two such therapies were recently approved by FDA. They are the first two gene therapies ever approved by FDA.
Cancer treatment is changing very quickly. Ask your doctor about the newest treatments for your type of cancer.
“It’s your right and responsibility to make sure you’re getting the right treatment, and that may involve wanting to get a second opinion,” LoRusso advises. Most doctors welcome a second opinion.
For tips on how to find a cancer specialist and learn about your treatment options, see the Wise Choices box.
Intel faces a big test: two serious security issues with its chips that could have implications for nearly everyone touched by computing. And so far Intel has failed to quiet critics, putting it in an awkward position this week as its chief executive prepares to take the stage at one of the world’s biggest tech trade shows. The cause of the public relations crisis is the disclosure of two new ways to filch data from the microprocessors.(New York Times)
Rivals including JPMorgan Chase and Bank of America are due to post their highest post-crisis annual net income during results season, which begins on Friday. In contrast, figures from Wells are expected to show how long it is taking to recover after thousands of its staff created up to 3.5 million bank and credit card accounts for customers without their permission. (Financial Times)
Wealthfront closed yet another round of funding. Along with news reports touting the firm’s $75 million capital inflow to help it develop new products for its growing client base, it inspired yet another round of skepticism from the traditional financial advice industry. Andy Rachleff, chief executive of Wealthfront, said the funding brought in by a group led by Tiger Global Management would be “more than enough” to turn the digital wealth management firm profitable.(InvestmentNews)
Denali Therapeutics and Takeda Pharmaceutical have agreed to work together to develop up to three drugs for neurodegenerative diseases, including a compound that could treat Alzheimer’s disease. The deal calls for Takeda to pay Denali $155 million, a combination of cash and stock purchases. If South San Francisco-based Denali successfully advances the compounds to human testing, the company could win $90 million more in payments.(Xconomy)
International Business Machines Corp. and Comcast Corp.’s venture arm will become the largest supporters of an investment fund for startups that help corporations use blockchain, the digital ledger that’s become a hot technology. The startup accelerator, called MState, plans to invest $25,000 to $50,000 apiece in five or six companies over the next six months, co-founder Rob Bailey said in a phone interview.(Bloomberg)
Tech companies working with augmented reality and virtual reality technologies raised more than $3 billion in venture funding in 2017. This data comes from analytics firm Digi-Capital and suggests that while the buzz surrounding the AR/VR space has tapered off, the sheer amount of cash getting pumped into the industry is continuing to surge.(TechCrunch)
Software on Apple Inc.’s iPhones and Google’s Android smartphones help mobile apps like Uber and Facebook to pinpoint a user’s location, making it possible to order a car, check in at a local restaurant or receive targeted advertising. But 911, with a far more pressing purpose, is stuck in the past. Better technology would be especially helpful, regulators say, when a caller can’t speak or identify his or her location.(Wall Street Journal)
The Renault-Nissan-Mitsubishi alliance is pooling $200 million in a new mobility tech fund, three sources said, in the latest move by major automakers to adapt to rapid industry change by investing in startups through their own venture capital arms. The fund is due to be unveiled by alliance chairman Carlos Ghosn at the CES tech industry show in Las Vegas on Tuesday.(Automotive News Europe)
For years, sales of domestic light beer have tanked as imbibers turn to craft brews, wine and spirits. Now an even bigger threat looms: the growing reality of legal, readily available and socially condoned marijuana. That doesn’t bode well for Anheuser-Busch InBev or MillerCoors, which has pledged to revitalize Coors Light and Miller Lite this year and next. One industry expert says the industry stands to lose 7.1 percent of its overall sales, or more than $2 billion.(Crain’s Chicago Business)
Most investment strategists think 2018 will go down in history as “not quite as good as 2017.” And that doesn’t mean it will be a bad year. But in 2017, stocks ran to 20 percent gains and volatility was as gentle as a newborn foal. Leading equity managers are betting on technology, with Fidelity’s Will Danoff explaining why stocks like Facebook and Amazon are in very different positions today than firms like Cisco and Oracle were back in 2000.(InvestmentNews)
Caffeine Level in Blood May Help Diagnose Parkinson’s
Summary: A new study to be released in Neurology identifies caffeine levels in the blood as a potential biomarker for Parkinson’s disease, Researchers discovered people with Parkinson’s had lower levels of caffeine in their blood than people without the disease, even if they had consumed the same amount of caffeine.
Source: AAN.
Testing the level of caffeine in the blood may provide a simple way to aid the diagnosis of Parkinson’s disease, according to a study published in the January 3, 2018, online issue of Neurology.
The study found that people with Parkinson’s disease had significantly lower levels of caffeine in their blood than people without the disease, even if they consumed the same amount of caffeine.
“Previous studies have shown a link between caffeine and a lower risk of developing Parkinson’s disease, but we haven’t known much about how caffeine metabolizes within the people with the disease,” said study author Shinji Saiki, MD, PhD, of Juntendo University School of Medicine in Tokyo, Japan.
People in the study with more severe stages of the disease did not have lower levels of caffeine in the blood, suggesting that the decrease occurs from the earliest stages of the disease, according to David G. Munoz, MD, of the University of Toronto in Canada, who wrote an editorial accompanying the study.
“If these results can be confirmed, they would point to an easy test for early diagnosis of Parkinson’s, possibly even before symptoms are appearing,” Munoz said. “This is important because Parkinson’s disease is difficult to diagnose, especially at the early stages.”
The study involved 108 people who had Parkinson’s disease for an average of about six years and 31 people of the same age who did not have the disease. Their blood was tested for caffeine and for 11 byproducts the body makes as it metabolizes caffeine. They were also tested for mutations in genes that can affect caffeine metabolism.
The two groups consumed about the same amount of caffeine, with an average equivalent to about two cups of coffee per day. But the people with Parkinson’s disease had significantly lower blood levels of caffeine and nine of the 11 byproducts of caffeine in the blood. The caffeine level was an average of 79 picomoles per 10 microliters for people without Parkinson’s disease, compared to 24 picomoles per 10 microliters for people with the disease. For one of the byproducts, the level was below the amount that could be detected in more than 50 percent of the people with Parkinson’s disease.
In the statistical analysis, the researchers found that the test could be used to reliably identify the people with Parkinson’s disease, with a score of 0.98 where a score of 1 means that all cases are identified correctly.
In the genetic analysis, there were no differences in the caffeine-related genes between the two groups.
Limitations of the study include that people with severe Parkinson’s disease were not included, which could affect the ability to detect an association between disease severity and caffeine levels. Munoz also noted that all of the people with Parkinson’s were taking Parkinson’s medication and it’s possible that these drugs could affect the metabolism of caffeine.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Funding: The study was supported by the Japan Agency for Medical Research and Development, Japan Society for the Promotion of Science, and the Japanese Ministry of Education, Culture, Sports, Science and Technology.
Source: Renee Tessman – AAN Publisher: Organized by NeuroscienceNews.com. Image Source: NeuroscienceNews.com image is in the public domain. Original Research: The study will appear in Neurology.
UCLA researchers investigated how the brain responds when people watch other experience painful events. The study reports neural responses predict whether people will be inclined to avoid causing harm to others when faced with moral dilemmas.…READ MORE…
Binghampton University researchers report sleeping less than 8 hours a night can result in negative, repetitive thoughts associated with anxiety and depression.…READ MORE…
A new study reveals Parkinson’s patients have more copies of mitochondrial DNA in the brain stem, leading to increased cell death within that area.…READ MORE…
UC Santa Barbara researchers reveal humans and fruit flies can sense the taste of calcium. The researchers have identified a unique class of gustatory receptor neurons required to help taste calcium in Drosophila.…READ MORE…
Researchers look at how sleep deprivation can impact cognition, information processing and memory. A new study reveals sleep deprived mice can demonstrate sleep like brain activity while awake.…READ MORE…
Summary: Deep brain stimulation to the nucleus accumbens can help prevent impulsive behaviors, researchers report in PNAS.
Source: Stanford.
Stanford University School of Medicine investigators have identified the smoking gun of a “moment of weakness”: a signature pattern of electrical activity in a small, deep-brain region just a second or two before a burst of impulsive behavior.
The Stanford scientists discovered similar patterns in mice that had learned to binge eat fatty food and in a human subject anticipating a large cash reward. The researchers also showed, in mice, that supplying a small electrical pulse to the brain region in question, called the nucleus accumbens, as soon as the electrical signature manifested prevented the mice from overindulging in fatty food, while not affecting their intake of normal food, their social behavior or other physical activity.
The findings were published online Dec.18 in the Proceedings of the National Academies of Sciences.
“We’ve identified a real-time biomarker for impulsive behavior,” said Casey Halpern, MD, assistant professor of neurosurgery and the study’s senior author. Postdoctoral scholar Hemmings Wu, PhD, and neurosurgery resident Kai Miller, MD, PhD, share lead authorship.
Good impulses gone bad
“Impulses are normal and absolutely necessary for survival,” Halpern said. “They convert our feelings about what’s rewarding into concrete action to obtain food, sex, sleep and defenses against rivals or predators.”
But in some contexts, impulsive behavior can be pathological, manifesting as a marked tendency to make poor decisions and act on them. One need look no further than the recent rash of reports of sexual predators perched in powerful positions in Hollywood, the media, finance and politics to see examples of a fundamentally healthy drive — sexual appetite — taken to a pathological level.
The nucleus accumbens is the hub of the brain’s reward circuitry, which evolution has engineered to reinforce survival-promoting actions by inducing pleasure in anticipation or performance of those actions. The study’s findings offer the promise, Halpern said, of an implantable device that monitors the nucleus accumbens for the telltale signal preceding a burst of impulsivity and immediately delivers a measured dose of electricity. This intervention may prevent impulsive and sometimes life-threatening actions by high-risk people for whom all noninvasive therapies have failed.
The findings could also lead to less invasive methods of countering obesity, substance-abuse disorders, pathological gambling, sexual addiction or intermittent explosive disorder, a psychiatric condition marked by impromptu outbursts of inappropriate ferocity.
“Imagine if you could predict and prevent a suicide attempt, a heroin injection, a burst of binge eating or alcohol intake, or a sudden bout of uncontrolled rage,” said Halpern.
Clinically, Halpern focuses on deep-brain stimulation, whereby devices deliver electrical pulses to targeted brain regions in which they’ve been implanted. DBS is now approved by the Food and Drug Administration for treating symptoms of Parkinson’s disease and essential tremor, and is currently in clinical trials for depression, obsessive-compulsive disorder and multiple other disorders of the brain.
But the tens of thousands of DBS devices in current use are inflexible in the timing, duration and intensity of the pulses they deliver; they simply fire away on a preprogrammed basis, 24/7. New-generation devices can respond to feedback from the brain region they target, or even a distant one, so pulses get delivered only when necessary and at appropriate intensities. These so-called responsive neurostimulation devices have so far been approved for partial-onset epilepsy. Because they fire only after sensing specific electrical-activity signatures, they may actually deliver as little as five minutes per day of total stimulation, which neuroscientists such as Halpern view as greatly advantageous from the standpoint of avoiding side effects and optimizing the behavioral specificity of the treatment.
“There’s no available responsive neurostimulation intervention for dangerous impulsive behavior yet, because until now no one’s been able to document a characteristic signature in the brain that could be used for triggering pulse delivery by the device,” he said.
From mouse to man
The Stanford scientists discovered this signature in experiments with mice. Typically, laboratory mice are fed pellets of a standard chow that’s nutritious without being highly caloric. In the study, mice were given special high-fat food pellets for one hour every day for 10 days. During that hour, they were allowed to eat as much as they wanted.
The novel food took some getting used to, but by day 10 the mice became habituated to it and pretty much ate it nonstop. The researchers had implanted electrode arrays in the mice’s brains in order to monitor electrical activity in the nucleus accumbens, where a pattern of heightened electrical activity — restricted to a particular low-frequency band called delta — emerged immediately prior to binge eating, peaking about one second before a mouse took a bite of the high-fat food pellet. Notably, this uptick didn’t occur when that mouse was about to bite into standard lab chow. Nor was it seen in other typically rewarding activities, such as interactions with younger mice.
Halpern and his colleagues then programmed their electrode arrays to deliver 10-second pulses of electrical current — the typical regimen in approved DBS therapies — to the nucleus accumbens whenever the arrays sensed a sizeable increase in delta intensity there. This substantially reduced the mice’s high-fat binges. But it didn’t affect their social lives, or their general physical behavior.
Further experiments compared responsive neurostimulation to standard DBS, random pulse delivery and manual delivery whenever an experimenter saw a mouse preparing to stuff itself. Both manual and responsive-neurostimulation pulse delivery proved superior to either random or DBS delivery, despite delivering far fewer electrical pulses daily than DBS.
Next, the Stanford researchers took advantage of a rare opportunity to perform a similar experiment on a human subject: a patient with obsessive-compulsive disorder, a condition for which DBS to the nucleus accumbens is in clinical trials. This participant was resistant to all other treatments for his OCD and had opted for surgical implantation of a DBS device.
The investigators received the participant’s consent to intervene briefly once electrical leads had been introduced to the participant’s nucleus accumbens but prior to their hookup with the DBS pulse generator. In the interim, the participant was asked to perform computerized tasks that generated cash rewards if completed successfully. As with the mice, once the participant got acclimated to the near-certainty of receiving a reward upon completing the task, a receiver to which the implanted electrical leads were temporarily hooked was able to detect the characteristic “high-delta” electrical signature in his nucleus accumbens just before he commenced the tasks.
“The fact that we saw a similar signal prior to two different behaviors, both intended to obtain rewards — food in the case of mice, money in the case of the human subject — to which the individuals had become hypersensitized by their repeated exposure suggests that this signal may be common to many impulsive behaviors, making them amenable to treatment along similar lines,” said Halpern.
Unlike newer parts of the brain, such as the cerebral cortex, the more deeply seated reward system’s components have largely been conserved among vertebrates. So Halpern thinks the behavior-altering results his team observed in mice are likely to apply to humans, although further study will be needed to confirm these findings in a single human subject.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Halpern, Wu and study co-author Robert Malenka, MD, PhD, professor of psychiatry and behavioral sciences, are co-authors of a provisional patent filed by Stanford’s Office of Technology Licensing on intellectual property associated with these findings.
Additional Stanford co-authors are former neurology research assistant Zack Blumenfield; visiting medical student Vinod Ravikumar; former undergraduate student Karen Lee; medical student Bina Kakusa; postdoctoral scholars Matthew Sacchet, PhD, and Daniel Christoffel, PhD; instructor of psychiatry and behavioral sciences Nolan Williams, MD; professors of radiology Brian Rutt, PhD, and Max Wintermark, MD; professor of neurology Helen Bronte-Stewart, MD; and professor of psychology Brian Knutson, PhD.
Halpern is a member of Stanford Bio-X and the Stanford Neurosciences Institute.
Funding: Funding for the study was provided by the National Institutes of Health (grants K12NS080223, UL1TR001085), the Brain & Behavior Foundation, the Neurosurgery Research and Education Foundation, the John A. Blume Foundation, the William Randolph Hearst Foundation, the European Society for Stereotactic and Functional Neurosurgery Research and the Stanford Neuroscience Institute’s Neurochoice Initiative.
Stanford’s Department of Neurosurgery also supported the work.
Source: Bruce Goldman – Stanford Publisher: Organized by NeuroscienceNews.com. Image Source: NeuroscienceNews.com image is credited to Miller et al./PNAS. Original Research: Full open access research for “Closing the loop on impulsivity via nucleus accumbens delta-band activity in mice and man” by Hemmings Wu, Kai J. Miller, Zack Blumenfeld, Nolan R. Williams, Vinod K. Ravikumar, Karen E. Lee, Bina Kakusa, Matthew D. Sacchet, Max Wintermark, Daniel J. Christoffel, Brian K. Rutt, Helen Bronte-Stewart, Brian Knutson, Robert C. Malenka, and Casey H. Halpern in PNAS. Published online December 18 2017 doi:10.1073/pnas.1712214114
Closing the loop on impulsivity via nucleus accumbens delta-band activity in mice and man
Reward hypersensitization is a common feature of neuropsychiatric disorders, manifesting as impulsivity for anticipated incentives. Temporally specific changes in activity within the nucleus accumbens (NAc), which occur during anticipatory periods preceding consummatory behavior, represent a critical opportunity for intervention. However, no available therapy is capable of automatically sensing and therapeutically responding to this vulnerable moment in time when anticipation-related neural signals may be present. To identify translatable biomarkers for an off-the-shelf responsive neurostimulation system, we record local field potentials from the NAc of mice and a human anticipating conventional rewards. We find increased power in 1- to 4-Hz oscillations predominate during reward anticipation, which can effectively trigger neurostimulation that reduces consummatory behavior in mice sensitized to highly palatable food. Similar oscillations are present in human NAc during reward anticipation, highlighting the translational potential of our findings in the development of a treatment for a major unmet need.
“Closing the loop on impulsivity via nucleus accumbens delta-band activity in mice and man” by Hemmings Wu, Kai J. Miller, Zack Blumenfeld, Nolan R. Williams, Vinod K. Ravikumar, Karen E. Lee, Bina Kakusa, Matthew D. Sacchet, Max Wintermark, Daniel J. Christoffel, Brian K. Rutt, Helen Bronte-Stewart, Brian Knutson, Robert C. Malenka, and Casey H. Halpern in PNAS. Published online December 18 2017 doi:10.1073/pnas.1712214114
Blueberry Vinegar Improves Memory in Amnesia: Mouse Study
Summary: A new study reports blueberry vinegar could be effective in restoring memory to mice suffering from induced amnesia. Researchers note, that while further testing needs to be completed, the fermented product could help restore cognitive function to those with dementia and age related cognitive decline.
Source: ACS.
Dementia affects millions of people worldwide, robbing them of their ability to think, remember and live as they once did. In the search for new ways to fight cognitive decline, scientists report in ACS’ Journal of Agricultural and Food Chemistry that blueberry vinegar might offer some help. They found that the fermented product could restore cognitive function in mice.
Recent studies have shown that the brains of people with Alzheimer’s disease, the most common form of dementia, have lower levels of the signaling compound acetylcholine and its receptors. Research has also demonstrated that blocking acetylcholine receptors disrupts learning and memory. Drugs to stop the breakdown of acetylcholine have been developed to fight dementia, but they often don’t last long in the body and can be toxic to the liver. Natural extracts could be a safer treatment option, and some animal studies suggest that these extracts can improve cognition. Additionally, fermentation can boost the bioactivity of some natural products. So Beong-Ou Lim and colleagues wanted to test whether vinegar made from blueberries, which are packed with a wide range of active compounds, might help prevent cognitive decline.
To carry out their experiment, the researchers administered blueberry vinegar to mice with induced amnesia. Measurements of molecules in their brains showed that the vinegar reduced the breakdown of acetylcholine and boosted levels of brain-derived neurotrophic factor, a protein associated with maintaining and creating healthy neurons. To test how the treatment affected cognition, the researchers analyzed the animals’ performance in mazes and an avoidance test, in which the mice would receive a low-intensity shock in one of two chambers. The treated rodents showed improved performance in both of these tests, suggesting that the fermented product improved short-term memory. Thus, although further testing is needed, the researchers say that blueberry vinegar could potentially be a promising food to help treat amnesia and cognitive decline related to aging.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Funding: The authors acknowledge funding from Konkuk University.
Source: Katie Cottingham – ACS Publisher: Organized by NeuroscienceNews.com. Image Source: NeuroscienceNews.com image is in the public domain. Original Research: The study will appear in Journal of Agricultural and Food Chemistry.
For some people, managing hypothyroidism isn’t just about taking medications. They also turn to vitamins and other nutrients for help in managing the condition, which occurs when the thyroid doesn’t make enough thyroid hormone.
“Vitamins and nutrients can help fight the underlying causes of thyroid disorders, such as autoimmune processes and inflammation, and help improve a dysfunctional thyroid,” says Raphael Kellman, MD, a functional medicine physician in New York City and author of “The Microbiome Diet.”
“You also want to make sure you have all the facts on the vitamins and minerals you’d like to supplement with,” says MaryAnne Metzak, RD, CDN, a registered dietitian at Staten Island University Hospital in New York. And it’s important to keep the lines of communication open between you and your doctor. “Your doctor needs to know exactly how much of each vitamin and supplement you’re taking in case you have a negative reaction,” Metzak says.
Specific nutrients that may be beneficial for hypothyroidism include:
Iodine. You need an adequate supply of iodine to make thyroid hormone. The recommended minimum iodine intake for most adults is 150 micrograms a day, according to the Office of Dietary Supplements. Good food sources include milk, cheese, poultry, eggs, kelp, and other seaweeds, Kellman says. “But you have to be careful with supplementing iodine because too much can be problematic and actually cause hypothyroidism,” he says.
Vitamin B. “Vitamin B is important for people with hypothyroidism because the B vitamins have many interactions with thyroid function and hormone regulation,” Metzak says. It’s best to take a nutritional supplement that includes the entire vitamin B complex, and you may need additional vitamin B12 if a blood test reveals your levels are low, she says. Good food sources of vitamin B include whole grains, legumes, nuts, milk, yogurt, meat, fish, eggs, seeds, and dark leafy greens.
Selenium. “Selenium supports efficient thyroid synthesis and metabolism,” says Denise Londergan, RD, MPH, a registered dietitian at Ohio State University’s Wexner Medical Center in Columbus. Foods that provide selenium include tuna, shrimp, salmon, sardines, scallops, lamb, chicken, beef, turkey, eggs, and shitake mushrooms. “Or you can take 100 to 200 micrograms of selenium in supplement form per day,” Kellman says.
Zinc. In addition to selenium, zinc plays a role in the conversion of the thyroid hormone T4 to T3. Metzak says selenium and zinc are beneficial in improving thyroid function and hormone levels. Food sources of zinc include shellfish, mollusks, meat, legumes, and nuts. “If you opt for a zinc supplement, 30 milligrams is sufficient,” Kellman says.
Tyrosine. “Tyrosine is a nutrient involved in thyroid hormone production and conversion,” Kellman says. One of the best ways to get more tyrosine, an amino acid, is to make sure you’re getting enough protein, Londergan says. Aim for 10 to 35 percent of your calories from protein each day.
Vitamin D. “Research has shown a strong association with vitamin D deficiency and people with hypothyroidism,” Metzak says. In a study published in the November 2013 issue of the International Journal of Health Sciences, researchers looked at the vitamin D levels of 30 people with hypothyroidism and 30 who didn’t have the condition and found that the vitamin D levels were significantly lower in those with hypothyroidism. You can get vitamin D from fortified milk, yogurt, and orange juice. “Food sources of vitamin D are often not adequate, however,” Kellman says. He recommends supplements for those who are vitamin D deficient. Your doctor can let you know if that’s necessary, and which dosage is best for you.
Probiotics. “The microbiome in the gut plays a critical role in many physiological processes, including thyroid function,” Kellman says. Because of this, he recommends taking a probiotic supplement. “I don’t necessarily recommend the supplement with the highest number of bacteria — although that’s important — but supplements with the most diversity,” he says. To get the maximum amount of different bacteria, Kellman recommends changing your probiotic supplement often.
As with any chronic condition, a healthy diet can go a long way with hypothyroidism. “Eat an anti-inflammatory diet full of lots of fruits and vegetables and unprocessed foods, and limit sugar,” Londergan says.
