Mycotoxins and Your Brain


Mycotoxins are toxins derived from mold. These toxins have the potential to harm and even kill.

Mycotoxin exposure can come from both dietary and environmental sources. Dietary sources include spoiled food and environmental sources include living or working in water-damaged buildings, airborne or physical contact with outdoor molds, and airborne dust in buildings containing mold spores.

Individuals most at risk for mycotoxin exposure include those who live or work in older buildings, those who have known exposure to water-damaged buildings, and those with impaired immune responses or higher levels of oxidative stress.

Unfortunately, molds are often overlooked despite the prevalence within our homes and workplace environments.

In fact, the CDC’s National Institute for Occupational Safety and Health reported that 50% of commercial and residential buildings are estimated to contain toxic mold.

Meet Steve…

I’d like to share a story about a man we’ll call Steve. Steve was suffering from brain fog, and as a senior executive for an oil company, it was impeding his ability to work at full mental capacity. It all began with a feeling of anxiousness and confusion. He could no longer do multiple projects at the same time, and his word recollection eluded him.

Symptoms had been interfering in his quality of life for approximately a year and a half to the point where Steve had already been to the Mayo Clinic twice and had been seen by other famous clinics. Test after test did not indicate any signs of disease, but he clearly was having dysfunction.

Within two minutes of Steve walking through my doors, I asked him, “When did your basement flood?”

What the tests didn’t reveal, his complexion did. Steve had mold toxicity. Confirmed with a simple urine test, his mold levels came back sky high. Two years prior, his basement had flooded. He had hired a team to get the water out quickly, but six months later began showing symptoms of mold toxicity.

Mold had established itself in his home, and he was breathing it in every day.

Symptoms of Mold and Mycotoxin Toxicity

Mycotoxins can lead to a number of serious health concerns, including autoimmune disease and cancer.

There may be a higher incidence of autoimmune or neurological symptoms with mycotoxin toxicity.

There are 37 different neurological and physiological complaints that are associated with exposure to mold. Steve’s primary complaints were confusion, feeling anxious, an inability to think clearly, difficulty focusing, and problems with word recollection.

Mycotoxin symptoms are often general or vague, and difficult to associate with a diagnosis or disease state, and, therefore, may be overlooked during clinical assessments.

Conditions and symptoms associated with mycotoxin exposure include:

  • Fatigue and weakness
  • Chronic burning in the throat and nasal passages
  • Coughing, wheezing, and shortness of breath
  • Loss of balance
  • Depression and/or anxiety
  • Skin rashes
  • Eye irritation or tearing of the eyes
  • Headache and/or light sensitivity
  • Hearing loss
  • Heightened sensitivity to chemicals and foods
  • Irregular heartbeat
  • Morning stiffness and/or joint pain
  • Muscle weakness
  • Sleep problems
  • Poor memory, difficulty finding words
  • Slower reaction time
  • Vision changes
  • Difficulty concentrating
  • Abdominal pain, diarrhea, and/or bloating
  • Unusual skin sensations, tingling, and numbness
  • Increased urinary frequency or increased thirst
  • Disorientation and/or dizziness
  • Static shocks or metallic taste in the mouth

Testing for Mycotoxin Exposure

The Vibrant Wellness Mycotoxins Test is a urine-based assay for 31 of the most common mycotoxins produced by molds. This test is measured on a microarray platform to produce the most accurate and clinically relevant assessment of difficult-to-detect toxins that can cause serious disease.

Mycotoxins measured in the test reflect past and recent mold exposure in the diet and environment. Mycotoxins can colonize in various body systems. It can be seen in dental plaque, nasal passages, vaginal and urinary infections, within the heart valves, in your gut, skin or in middle ear infections. Some molds have the ability to form biofilms.

Biofilms can help offer a protective shield for the mycotoxins to colonize, such as in the nasal cavities. Biofilms can offer shelter to Lyme disease.

Results cannot determine timing or duration of exposure. However, the report does indicate whether the mycotoxin measured is a metabolite of food or environmental mold. The interpretive challenges for clinicians and patients are determining, and remediating, the source of environmental mold exposure.

Due to the common co-occurrence of Lyme and mycotoxin exposure from depressed immunity in affected individuals, as well as symptom overlap between tickborne diseases and mycotoxins, consider running the vibrant tickborne diseases panel along with the Vibrant Mycotoxins test.

Getting To The Root Of The Problem

The chemicals and spores released by mold disrupt your immune system and cause inflammation. It can cause infections to occur anywhere in your body; however, your brain is notoriously vulnerable to mold.

Kitchens and bathrooms are most closely associated with mold and mycotoxins. Think about the tracks along the shower door, your shower curtains, dripping water, and crevices that water seeps into. You could also be breathing it in through ventilation shafts. It could be lurking within and beneath your carpeting. And like Steve and so many others, it could be from a flooded basement.

I sent Steve home with directives to get a mold remediation specialist to eliminate the repeated exposure to the mold endotoxins that could be lurking in the drywall, his heating and cooling systems, his air filtration unit, and in those dark corners.

When you search for mold, don’t forget to look outside as well. It can even enter your house through the insulation from a leak on the outside of your house. Whether you live in a hot or cold climate or a wet or dry climate, mold exists. And when it is lurking in your home, just like Steve, you are repeatedly breathing it in.

How to Regain Your Brain After Mycotoxin Exposure

I gave Steve the protocols I use in my book You Can Fix Your Brain and in my “Brain Masterclass” to help him regain his brain health. A few months later, he reported a vast improvement. His mental clarity had returned, and with it his confidence at work.

Because of the ability for these molds and mycotoxins to colonize, you can rid your environment of mold and still continue to breathe in mold everyday if it set up shop in the lining of your nasal passages. This means that you need to break up the biofilms that coat and protect the toxins in order to take it that one step further.

In my book You Can Fix Your Brain, the subheading is “Just One Hour a Week to the Best Memory, Productivity, and Sleep You’ve Ever Had.” That’s not a cutesy title I picked out. It’s the best method I have found for making substantive change and improving your health. Inch by inch, always moving forward, keeping your eye on the prize – your health.

One of the things you have to keep in mind is that while your body is fighting off the exposure to mold and mycotoxins, it is still having to deal with all the other toxins you come in contact with. The sad reality is that we are living in toxic soup, and it is up to us to clean up our little piece of the world. It isn’t just mold that your body has to deal with. It’s the toxins in your shampoo, detergent, air, plastics, water, and food.

So while it is imperative that you eliminate the mold immediately, you also need to help support your immune system by eliminating some of the other assaults against it in order to reduce your toxic burden.

I created a course that was a complementary resource for the book You Can Fix Your Brain.  In my “You Can Fix Your Brain Masterclass”, I provide you with tools that help you learn where to look for those environmental toxins in your home, and teach you how to make simple swaps to support the health of every single person that lives in that home. It’s not just you that breathes in that mold. Anyone that enters that house does, and some people have a deadly allergy to it.

Why Functional Medicine Is Superior

We don’t need to stay sick. Steve could’ve taken a pill for anxiety or a pill to help him focus, but he still would’ve been breathing in toxins every day. They would’ve kept accumulating doing more and more damage until one day, it isn’t brain fog; it’s dementia or fibromyalgia or respiratory problems.

Steve was smart. He sought out the reason behind the symptoms. He got to the root cause and eliminated it. He applied a few practical strategies and allowed his body to do what it was so eloquently designed to do: heal.

The way that our immune system protects us, and this is true not just for humans, but for every living species on the planet, is with an innate immune system, meaning it’s built into the body. It’s innately there as part of life and the innate immune system creates cytokines. They’re like bullets to attack whatever it considers to be a foreign agent, something that’s a threat. What’s important for humans to understand is that we have the exact same body as our ancestors did thousands of years ago. We use our brains more and we’ve developed more creature comforts, but we have the exact same body functions as our ancestors. What did our ancestors’ immune systems have to protect them from? Bugs, parasites, viruses, molds, fungus and bacteria. That was it.

Your body is capable of fighting mold. If you accidentally ingest it or inhale it, it initiates this response. However, if your body continues to breathe this in, your body calls for a stronger defense. This is for chronic insults that your innate immune system felt it could not protect you from well enough to snuff out the problem.

This is when we see chronic conditions occur, like chronic sinusitis, or cognitive dysfunction.

So many people struggle for years with symptoms. They look at the symptoms as the disease — they have it backwards. The disease is a symptom. It’s your body crying out for you to stop whatever it is that is causing the problem so it can resume the day-to-day healing.

Once you have this paradigm shift, health care is never the same. You begin to ask the right questions that help you attain health instead of treating disease. And, like Steve, you actively choose not to go down that rabbit hole of taking pills that help you focus while you continue to subject yourself to mold and mycotoxins as they destroy your brain.

You’ll start to ask the question, “What is the root cause of this symptom I am experiencing?” Then you can address the real problem (the mold), not just the symptoms (brain fog, anxiety, and the many other symptoms caused by mold and mycotoxin exposures).

Ascending Thoracic Aortic Aneurysms: A ‘Silver Lining’?


Aortic Aneurysms:

Often known as a “silent killer,” ascending thoracic aortic aneurysms (ATAAs) may grow asymptomatically until they rupture, at which point, mortality is over 90%.

But ATAAs may also carry a potential flip side: Apparent protection against the development of atherosclerotic plaque and by extension, for those who have one, a significantly reduced risk for coronary artery disease and myocardial infarction (MI).

“We noticed in the operating room that many patients we worked on who had an ATAA had pristine arteries, like a teenager’s,” John Elefteriades, MD, William W.L. Glenn Professor of Cardiothoracic Surgery and former chief of cardiothoracic surgery at Yale University and Yale New Haven Hospital, New Haven, Connecticut, told theheart.org | Medscape Cardiology. “The same was true of the femoral artery, which we use to hook up to the heart-lung machine.”

Elefteriades and colleagues have been investigating the implications of this association for more than two decades. Many of their studies are highlighted in a recent review of the evidence supporting the protective relationship between ATAAs and the development of atherosclerosis and the possible mechanisms driving the relationship.

“We see four different layers of protection,” Sandip Mukherjee, MD, medical director of the Aortic Institute at Yale New Haven Hospital and a senior editor of the journal AORTA, told theheart.org | Medscape Cardiology. Mukherjee collaborated with Elefteriades on many of the studies.

The first layer of protection is lower intima-media thickness, specifically, 0.131 mm lower than in individuals without an ATAA. “It may not seem like very much, but one point can actually translate into a 13%-15% decline in the rate of myocardial infarction or stroke,” Mukherjee said.

The second layer is lower levels of low-density lipoprotein (LDL) cholesterol. Lower LDL cholesterol levels (75 mg/dL) were associated with increased odds of ATAAs (odds ratio [OR], 1.21), whereas elevated levels (150 mg/dL and 200 mg/dL) were associated with decreased odds of ATAAs (OR, 0.62 and 0.29, respectively).

Lower calcification scores for the coronary arteries are the third layer of protection (6.73 vs 9.36 in one study).

The fourth protective layer is a significantly reduced prevalence of coronary artery disease. A study of individuals with ATAA compared to controls found 61 of those with ATAA had coronary artery disease vs 140 of controls, and 11 vs 83 had experienced an MI. Of note, patients with ATAAs were protected despite having higher body mass indices than controls.

Other MI risk factors such as age increased the risk even among those with an ATAA but, again, much less so than among controls; a multivariable binary logistic regression of data in the team’s review showed that patients with ATAAs were 298, 250, and 232 times less likely to have an MI than if they had a family history of MI, dyslipidemia, or hypertension, respectively.

Why the Protection?

The ligamentum arteriosum separates the ascending from the descending (thoracoabdominal) aorta. ATAAs, located above the ligamentum, tend to be pro-aneurysmal but anti-atherosclerotic. In the descending aorta, below the ligamentum, atherosclerotic aneurysms develop.

The differences between the two sections of the aorta originate in the germ layer in the embryo, Elefteriades said. “The fundamental difference in tissue of origin translates into marked differences in the character of aneurysms in the different aortic segments.”

What specifically underlies the reduced cardiovascular risk? “We don’t really know, but we think that there may be two possible etiologies,” Mukherjee said. One hypothesis involves transforming growth factor–beta (TGF-beta), which is overexpressed in patients with ATAA and seems to increase their vulnerability to aneurysms while also conferring protection from coronary disease risk.

Some studies have shown differences in cellular responses to TGF-beta between the thoracic and abdominal aorta, including collagen production and contractility. Others have shown that some patients who have had an MI have polymorphisms that decrease their levels of TGF-beta.

Furthermore, TGF-beta plays a key role in the development of the intimal layer, which could underpin the lack of intimal thickening in patients with ATAA.

But overall, studies have been mixed and challenging to interpret, Elefteriades and Mukherjee agreed. TGF-beta has multiple remodeling roles in the body, and it is difficult at this point to isolate its exact role in aortic disease.

Another hypothesis involves matrix metalloproteinases (MMPs), which are dysregulated in patients with ATAA and may confer some protection, Mukherjee said. Several studies have shown higher plasma levels of certain MMPs in patients with ATAAs. MMPs also were found to be elevated in the thoracic aortic walls of patients with ATAA who had an aortic dissection, as well as in the aortic smooth muscle cells in the intima and media.

In addition, some studies have shown increased levels of MMP-2 in the aortas of patients with ATAAs compared with patients with coronary artery disease.

Adding to the mix of possibilities, “We recently found a gene that’s dysregulated in our aneurysm patients that is very intimately related to atherosclerosis,” Elefteriades said. “But the work is too preliminary to say anything more at this point.”

“It would be fabulous to prove what it is causing this protection,” Mukherjee added. “But the truth is we don’t know. These are hypotheses.”

“The most important message from our work is that most clinicians need to dissociate an ATAA from the concept of atherosclerosis.” Elefteriades said. “The ascending aorta is not an atherosclerotic phenomenon.”

How to Manage Patients With ATAA

What does the distinct character of ATAAs mean for patient management? “Finding a drug to treat ATAAs — to prevent growth, rupture, or dissection — has been like a search for the Holy Grail,” Elefteriades said. “Statins are not necessary, as this is a non-atherosclerotic process. Although sporadic studies have reported beneficial effects from beta-blockers or angiotensin II receptor blockers (ARBs), this has often been based on ‘soft’ evidence, requiring a combination of outcome measures to achieve significance.”

That said, he noted, “The mainstay, common sense treatment is to keep blood pressure controlled. This is usually achieved by a beta-blocker and an ARB, even if the benefit is not via a direct biologic effect on the aneurysmal degenerative process, but via simple hemodynamics — discouraging rupture by keeping pressure in the aorta low.”

Mukherjee suggested that these patients should be referred to a specialty aneurysm center where their genes will be evaluated, and then the aneurysm will be followed very closely.

“If the aneurysm is larger than 4.5 cm, we screen the patient every single year, and if they have chest pain, we treat them the same way as we treat other aneurysms,” he said. “As a rule of thumb, if the aneurysm reaches 5 cm, it should come out, although the size at which this should happen may differ between 4.5 cm and 5.5 cm, depending on the patient’s body size.”

As for lifestyle management, Elefteriades said, “Protection from atherosclerosis and MI won’t go away after the aneurysm is removed. We think it’s in the body’s chemistry. But even though it’s very hard for those patients to have a heart attack, we don’t recommend they eat roast beef every night — although I do think they’d be protected from such lifestyle aberrations.”

For now, he added, “Our team is on a hunt to find a drug to treat ascending disease directly and effectively. We have ongoing laboratory experiments with two drugs undergoing investigation at some level. We hope to embark soon on clinical trials.”

‘A Milestone’

James Hamilton Black III, MD, vice chair of the writing committee for the 2022 American College of Cardiology/American Heart Association Aortic Disease Guideline and chief of Division of Vascular Surgery and Endovascular Therapy at Johns Hopkins Medicine, Baltimore, commented on the review and the concept of ATAA’s atherosclerotic protection for theheart.org | Medscape Cardiology.

“The association of ascending aortic aneurysms with a lower risk for MI is an interesting one, but it’s probably influenced, at least in part, by the patient population.” That population is at least partially curated since people are coming to an academic center. In addition, Black noted, “the patients with ATAAs are younger, and so age may be a confounding factor in the analyses. We wouldn’t expect them to have the same burden of atherosclerosis” as older patients.

Nevertheless, he said, “the findings speak to an emerging body of literature suggesting that although the aorta is a single organ, there are certainly different areas, and these would respond quite differently to environmental or genetic or heritable stressors. This isn’t surprising, and there probably are a lot of factors involved.”

Overall, he said, the findings underscore “the precision medicine approaches we need to take with patients with aortic diseases.”

In a commentary on the team’s review article, published in 2022, John G.T. Augoustides, MD, professor of anesthesiology and critical care at the Perelman School of Medicine in Philadelphia, Pennsylvania, suggested that ATAA’s “silver lining” could advance the understanding of thoracic aortic aneurysm (TAA) management, be integrated with the expanding horizons in hereditary thoracic aortic disease, and might be explored in the context of bicuspid aortic valve disease.

Highlighting the “relative absence” of atherosclerosis in ascending aortic aneurysms and its importance is a “milestone in our understanding,” he concluded. “It is likely that future advances in TAAs will be significantly influenced by this observation.”

Drug-Eluting Scaffold for Infrapopliteal Disease


In the trial by Varcoe et al., how did the use of a drug-eluting resorbable scaffold compare with angioplasty?

Among patients with chronic limb-threatening ischemia (CLTI) and infrapopliteal artery disease, angioplasty has been associated with frequent reintervention and adverse limb outcomes from restenosis. Varcoe et al. conducted a single-blind, randomized, controlled trial to evaluate the safety and efficacy of a new everolimus-eluting resorbable scaffold for the treatment of infrapopliteal artery disease in patients with CTLI.

Clinical Pearls

Q: What are the challenges of using angioplasty for infrapopliteal artery revascularization?

A: Several trials have evaluated methods for revascularization in the infrapopliteal circulation in an attempt to avoid the poor patency outcomes seen with angioplasty. However, most of these methods have failed because of the complex nature of the atherosclerotic disease and the difficulty of maintaining patency in both the short term and the long term. The challenges associated with infrapopliteal artery revascularization include extensive medial calcinosis, long lesion lengths, acute lesion recoil, and a predilection for flow-limiting dissection after angioplasty.

Q: Have drug-eluting devices been used to treat infrapopliteal artery disease?

A: Drug-eluting devices that inhibit neointimal hyperplasia have not been used routinely for the treatment of infrapopliteal artery disease. In numerous trials of drug-coated balloons and drug-eluting scaffolds and stents, the treatment has not resulted in greater patency than angioplasty or has had practical limitations. Of all the available approaches, the use of coronary drug-eluting stents with sirolimus analogues in below-the-knee interventions has shown the most promise for maintaining primary patency. However, the permanent nature of these metal implants has made some clinicians wary of their routine use.

Morning Report Questions

Q: What are the potential advantages of using a drug-eluting resorbable scaffold for infrapopliteal artery disease?

A: Drug-eluting resorbable scaffolds have potential advantages that may make them suitable for the treatment of infrapopliteal artery disease, and observational studies have shown promising results. Drug-eluting resorbable scaffolds have unique scaffolding properties that allow them to overcome mechanical failure while acting as a delivery platform for an antiproliferative drug during the restenotic phase after intervention. These scaffolds also undergo resorption over time, which facilitates vessel remodeling and potentially reduces the late complications associated with permanent metal stents.

Q: In the trial by Varcoe et al., how did the use of a drug-eluting resorbable scaffold compare with angioplasty?

A: For the primary efficacy end point (freedom from amputation above the ankle of the target limb, occlusion of the target vessel, clinically driven revascularization of the target lesion, and binary restenosis of the target lesion at 1 year), the Kaplan–Meier estimate was 74% in the scaffold group and 44% in the angioplasty group, with an absolute difference of 30 percentage points (95% confidence interval [CI], 15 to 46; one-sided P<0.001 for superiority). The primary safety end point (freedom from major adverse limb events at 6 months and perioperative death) was observed in 165 of 170 patients in the scaffold group and 90 of 90 patients in the angioplasty group, with an absolute difference of -3 percentage points (95% CI, -6 to 0; one-sided P<0.001 for noninferiority). The use of the scaffolds in the trial was restricted to the proximal two thirds of the infrapopliteal arteries. Caution must be used in extrapolating these findings to other anatomical locations.

Many Diseases Might Be Caused by Mitochondrial Dysfunction, 4 Ways to Prevent.


Mitochondria have a double-membrane structure.

The impact of mitochondria on health has received increasing attention in recent years. Mitochondria affect the quality of life and the rate of aging; hence, protecting mitochondria can prevent aging and chronic diseases, and even fight cancer.

According to a paper in the journal Molecular Basis of Disease, metabolic abnormalities are prevalent in many chronic diseases such as cardiovascular diseases, obesity, diabetes, and even cancer, and mitochondria play a central role in energy metabolism.

Mitochondria Are the Power Plants of the Cell

Mitochondria are small organelles in the cells. They are very small, typically between 0.75 and 3 microns, and cannot be seen under a microscope unless it is stained.

The number of mitochondria in each cell varies, ranging from a few hundred to a few thousand. Cells with high energy demands, such as liver cells and cardiac muscle cells, tend to have more mitochondria.

Mitochondria, aptly called a “cell’s power plant” and “energy factory,” is the main site of ATP (energy currency of the cell) production. Mitochondria use oxygen to further process glucose and fatty acids from food, thereby generating ATP that powers metabolic processes. Mitochondria in cells produce 90 percent of the energy our bodies need to function, according to the Molecular Basis of Disease paper. The average cell uses 10 billion ATP per day, while a typical adult requires 3.0×1025 ATP per day.

Mitochondria have a double-membrane structure.
Mitochondria have a double-membrane structure.

Mitochondria must function stably because our bodies cannot store ATP. At any given moment, a person has about 250 grams of ATP in their cells, which equates to 4.25 watts, or the energy stored in a single AA battery, and a healthy person will generate up to 1200 watts of energy per day.

Mitochondria also control apoptosis in cells.

Cells have life cycles; as they decline in function and become senescent, they enter a phase of destruction and clearance, also known as apoptosis.

Mitochondria determine which cells need to undergo apoptosis, in which case, they release a substance that activates the enzymes responsible for apoptosis, causing the cell to enter the apoptotic process.

Cancer cells can multiply and grow indefinitely because the apoptosis mechanism has failed. Apoptosis requires ATP; if the energy supply does not meet the cell’s needs, it cannot carry out the process.

Mitochondria also maintain the stability of calcium in the body and generate heat.

Mitochondria Are Susceptible to Damage and Are Associated With Various Diseases

Mitochondria are fragile. Mitochondrial function can be affected by factors such as viral infection, inflammation, certain nutrient deficiencies, chemical toxins, heavy metals, radiation, etc.

Mitochondria are also susceptible to oxidative damage from within—that is, damage caused by free radicals (also known as reactive oxygen species), a byproduct of mitochondrial metabolic processes. For example, mitochondria produce more energy when we eat, and more free radicals are generated as a result.

All of these factors will damage mitochondria or interfere with their ability to repair. When the mitochondria sense these threats, they will shut down the energy factories and alert the nucleus of the danger. At this point, mitochondrial function shifts from energy production to cellular defense.

Dr. Michael Chang, founder and attending physician of the Healed and Whole Clinic in California and the author of the book Mitochondrial Dysfunction: a Functional Medicine Approach to Diagnosis and Treatment, emphasized in an interview with The Epoch Times that the two functions of mitochondria are mutually exclusive, and they can only perform one of the two functions—once the energy-generating mechanism in the mitochondria changes or malfunctions, we are in trouble.

Cells with malfunctioning mitochondria will become starved of energy. The symptoms that people experience can vary greatly depending on the cell type.

These symptoms range from mild fatigue, sleep disturbances, decreased stamina, mood swings, and muscle and joint pain, to severe fatigue, brain fog, anxiety, depression, and heart and respiratory problems. Age-related degenerative conditions, such as hearing and vision loss and skin wrinkles, are also linked to mitochondria. Some other common diseases involving mitochondrial dysfunction include diabetes, cardiovascular disease, neurodegenerative disease, aging, chronic fatigue syndrome, fibromyalgia, infertility, and even cancer.

According to Chang’s estimation, about 50 percent of his patients have mitochondrial dysfunction, and the symptoms of these patients are diverse. The first symptom may be fatigue, while other symptoms include hormonal imbalance, which occurs because cells lack the energy to function properly. Many people also develop brain fog, because the brain is a high-energy-consuming organ. Some people may also show symptoms of cardiac dysfunction, such as heart failure.

Ways to Prevent Mitochondrial Dysfunction

1. Try to stay away from harmful factors that damage mitochondria

This is the first thing to keep an eye on if you want to keep your mitochondria healthy. Avoid:

It should be noted that stress and negative emotions can also affect the health of mitochondria, and they should be dealt with promptly.

2. Take nutritional supplements that mitochondria need, such as coenzyme Q10

Coenzyme Q10 is a key cofactor required for the functioning of mitochondria and an important component of cellular respiration. It is also a powerful antioxidant that affects cell signaling, metabolism, and energy transport. Many clinical trials have proven that coenzyme Q10 promotes energy production and reduces fatigue.

In a Spanish study, patients with fibromyalgia were randomly divided into two groups, one of which took 300 mg of coenzyme Q10 per day for 40 days. Compared with the placebo group, the coenzyme Q10 group experienced an approximately 52 percent reduction in fibromyalgia symptoms, with the most significant reduction in pain at 52 percent, fatigue at 47 percent, and morning tiredness at 44 percent.

A meta-analysis published in August 2022 showed that coenzyme Q10 can significantly reduce fatigue. Moreover, the group that took only coenzyme Q10 demonstrated a significant fatigue-alleviating effect compared to those who also took other nutritional supplements.

3. Adopt a ketogenic diet and intermittent fasting

Aging-related diseases and many chronic diseases, including cancer, are linked in some way to mitochondrial dysfunction.

Thomas N. Seyfried, a well-known scholar in cancer research and a professor of biology at Boston College, said in an interview with The Epoch Times that cancer is not a genetic disease, but a metabolic disease; and cancer is the result of cellular metabolism disorder. The mitochondrial metabolism of cancer cells is different from the efficient aerobic respiration used by normal cells. It does not use oxygen and produces much less ATP, while cancer cells can only obtain energy by decomposing glucose and glutamine.

Chang mentioned in his book that diabetes can be reclassified as a metabolic disorder rather than an endocrine disease. This is because the root of the problem is not insulin resistance, but mitochondrial dysfunction. When mitochondria fail to function properly, the rate of fat oxidation and energy production will drop, resulting in fat accumulation in our muscles and liver. These fats are converted to lipid peroxides that are cytotoxic, which further damage the mitochondria. Decreased mitochondrial function in beta cells also slows insulin secretion, leading to impaired glucose tolerance, hyperglycemia, and eventually Type 2 diabetes.

The ketogenic diet switches the mitochondria from burning glucose to burning ketone bodies, which produces relatively less toxic substances in the form of free radicals. Ketone bodies are a relatively cleaner fuel for mitochondria. Furthermore, cancer cells cannot metabolize ketone bodies. Therefore, the purpose of the ketogenic diet is to cut off the rations of cancer cells so that cancer can be reversed.

Intermittent fasting is good for the mitochondria. This is because, if we are constantly eating, the mitochondria have to keep burning fuel. Chang described it as like leaving the car engine running all the time and producing a lot of exhaust even though you are not traveling. Mitochondria build up damaging free radicals when they are constantly working. Intermittent fasting also keeps blood from rushing to the digestive tract to aid digestion; the gut can rest and its cells have a chance to repair themselves.

In addition, intermittent fasting can stimulate cells and mitochondria to start autophagy—like performing a spring cleaning—and form new mitochondria.

In addition to choosing unprocessed, natural, and organic foods, Chang suggested that we should relax and eat slowly with gratitude at mealtimes, as it can reduce internal stress, protect mitochondria, and help digestion.

4. High-intensity interval training is more beneficial for mitochondria

High-intensity interval training (HIIT) is good for mitochondrial health
High-intensity interval training (HIIT) is good for mitochondrial health.

Chang said that compared with low- and medium-intensity exercise, high-intensity interval training is relatively more beneficial to mitochondria. Besides, short bursts of high- and low-temperature stimulation, such as in saunas and cold baths, can stimulate mitochondria and boost their function.

Exercises like a long jog on a treadmill are not necessarily ideal. Chang explained that this may elevate stress hormones and also exhaust the mitochondria due to prolonged work.

Diseases Take Flight with Climate Change


The changing climate is providing opportunities for insects and other animals to spread infectious diseases to new populations

In September 2018, Gaurab Basu received an email alerting him that one of his patients, a man in his late 60s, had just been hospitalized with unexplained fever and confusion. Basu, an HMS instructor in medicine, primary care physician, and co-director of the Center for Health Equity Education and Advocacy at Cambridge Health Alliance, suspected that his patient might have an infection, but the cause was unclear. “It took some real detective work to figure out what it was,” Basu says. A lumbar puncture finally pinpointed the source of his patient’s malaise: West Nile virus, a mosquito-borne pathogen more common to the tropics than New England in early autumn. Basu had never encountered the virus in any of his patients and says the diagnosis “came as a real surprise.”

All over the world, doctors like Basu are contending with the consequences of significant changes in the distribution and prevalence of vector-borne infectious diseases. West Nile fever surfaced in the United States in 1999 and has since become the country’s most common mosquito-borne illness, affecting thousands of people every year. The disease is also spreading into Europe, along with other mosquito-borne diseases such as dengue and chikungunya, while in Africa malaria is moving into higher elevations.

Tick-borne diseases are also on the move. Cases of Lyme disease, anaplasmosis, and Powassan encephalitis have more than doubled throughout the United States throughout the past two decades, as the ticks that transmit these illnesses expand into new areas, according to Ben Beard, deputy director of the Division of Vector-Borne Diseases at the U.S. Centers for Disease Control and Prevention in Fort Collins, Colorado.

Several factors explain these trends, not least among them demographic and land-use changes that bring people and infectious disease vectors closer together. “But many models suggest that temperature is a dominant driver,” says Jason Rohr, an infectious disease biologist and chair of the Department of Biological Sciences at the University of Notre Dame.

“A disease that becomes more prevalent and severe in one place may become less so somewhere else and another may reveal a different temporal and geographic pattern.”

Critical aspects of a vector’s lifecycle, such as its growth, reproductive capacity, and biting rates, are temperature dependent. Temperature also influences rainfall patterns that in turn affect vector habitats. In general, mosquitoes lay eggs in standing water, and ticks thrive in humid weather. For them, “drought is death,” says Sam Telford, professor of infectious disease and global health at the Cummings School of Veterinary Medicine at Tufts University.

As global mean temperatures rise steadily with climate change, efforts to model and predict future trajectories for vector-borne diseases are taking on a new urgency. Climate “profoundly influences the effectiveness of different kinds of health interventions,” says Matthew Bonds, an associate professor of global health and social medicine in the Blavatnik Institute at HMS. “By modeling the complex interactions of multiple hosts, viruses, and temperature, we seek to identify the most effective strategies for reducing the risk of disease emergence.”

Temperature creep

That climate contributes to the spread of infectious diseases has long been known. In ancient Rome, for example, aristocrats would retreat to hillside resorts in summer to avoid malaria, a disease whose name derives from the Latin mal + aria, or “bad air.”

Now climate change is affecting the infectious disease landscape in profound ways. Greenhouse gases resulting from the burning of fossil fuels have pushed mean global temperatures higher by just over 1°C since 1850. If the most recent projections from the United Nations Intergovernmental Panel on Climate Change (IPCC) hold true, global average temperatures could rise by more than 1.5°C over the next 20 years, leading to dramatically higher sea levels; longer and more frequent heat waves; and extreme weather events, which are unusually severe weather or climatic conditions that, according to the U.S. Department of Agriculture, devastate communities and agricultural and natural ecosystems.

portrait of David Relman
David Relman
 

According to the IPCC, each incremental increase in global temperatures will lead to more deaths from infectious diseases and other causes. Yet not all vector-borne diseases will respond in the same way, or uniformly, to increases in mean global temperatures, says David Relman, MD ’82, the Thomas C. and Joan M. Merigan Professor in Medicine and professor of microbiology and immunology at Stanford University. As the climate warms, “a disease that becomes more prevalent and severe in one place may become less so somewhere else and another may reveal a different temporal and geographic pattern,” he notes. In 2008, Relman was the chair of the National Academy of Sciences panel that examined how climate change and extreme weather could affect the emergence of infectious diseases.

Rohr agrees, adding that many scientists have abandoned what was once a basic assumption in infectious disease modeling, namely, that a vector’s performance, that is, its capacity to thrive and infect people, increases linearly with rising temperature. Current models, Rohr says, which capture nonlinear relationships between warming and performance better than previous models, show that transmission of disease increases with rising temperatures—up to a point. Excessive heat beyond what vectors and pathogens can tolerate can slow transmission “and then diseases begin to decline,” Rohr says.

Peter Hotez, dean for the National School of Tropical Medicine and professor of pediatrics and molecular virology and microbiology at Baylor College of Medicine, points out that in certain parts of east Africa, skyrocketing temperatures and diminishing rainfall patterns are adversely affecting the mosquitoes that carry malaria and the snails that carry schistosomiasis. Yet temperature increases at higher elevations may create new niches for vector-borne pathogens, further contributing to the redistribution of mosquito- and snail-borne diseases.

Rohr and his colleagues recently published modeling results showing that the transmission of West Nile and five other mosquito-borne viruses peaks between 23°C and 26°C before dropping off as temperatures increase. According to the model’s predictions, transmission seasons will lengthen where cooler areas get warmer and contract in areas where the current temperatures already bump up against the vectors’ thermal limits. The model also shows that warming can boost transmission in higher elevations, where cool temperatures ordinarily keep vector populations in check.

Temperature increases at higher elevations may create new niches for vector-borne pathogens.

That is concerning especially for malaria transmission risk in the highlands of east Africa, which stretch over an area the size of Egypt south of the Sahara desert. Reaching heights of at least 1,500 meters, the highlands tend to be cool, with daily mean temperatures below 20°C. Malaria transmission occurs only seasonally in the region, and because of that, people who reside there are less likely to build an immunity to the disease than people in lower-lying areas where infections occur year-round.

With climate change, however, “I think malaria transmission in the highlands will increase,” says Marcia Castro, Andelot Professor of Demography and chair of the Department of Global Health and Population at the Harvard T.H. Chan School of Public Health. “Over time, those areas will become more susceptible to the mosquito vector staying longer than just a few months of the year.”

Predicting how warming affects malaria transmission is challenging, however, because climatic pressures often occur in tandem with land-use changes and health interventions that affect local disease rates. Indeed, deaths from malaria declined 40 percent in Africa between 2000 and 2015, largely because of the expanded use of insecticide-treated bed nets.

While a postdoc at the Harvard Chan School, Pamela Martinez, now an assistant professor of microbiology and statistics at the University of Illinois Urbana-Champaign and a visiting scientist at the Chan School, collaborated on a project to isolate the effects of temperature on the number of malaria cases in the highlands of Ethiopia. Malaria cases had surged in the highlands during the 1970s but by the beginning of the twenty-first century, the number of cases in the region had mysteriously fallen off. Martinez and her colleagues knew that efforts to protect local populations from infection had ramped up only in 2005, years after the incidence had begun trending downward. So public health interventions were not the likely reason for the decrease.

As it happened, however, the slowdown coincided with a multiyear pause in global warming between 1998 and 2005. During that time, mean global surface temperatures hardly budged, a phenomenon that scientists now attribute to transient and unusually strong oscillations in oceanic currents—El Niño in 1997-1998 and La Niña in 1998-1999—that led to the sea absorbing more heat from the atmosphere than normal.

Martinez and her colleagues suspected that the pause in global warming and the slowdown in malaria transmission were connected. Regional climate records confirmed that local temperatures had dropped in tandem with global averages during the period. When they modeled the data, the scientists found that climate conditions and the decrease in malaria cases were strongly coupled. Martinez says the findings underscore the crucial role of temperature in driving the incidence of malaria either lower or higher.

Warming also expands opportunities for disease transmission by other tropical pathogens, such as the Zika virus. Transmitted by the Aedes aegypti mosquito, the Zika virus had been common only in a narrow equatorial range in Africa and Asia. After 2007, however, the virus began spreading eastward across the Pacific Ocean. Since then, more than 80 countries have reported Zika outbreaks. An outbreak that began in Brazil in 2015 led to an estimated 1.5 million infections in that country before spreading elsewhere in the Americas. Zika typically produces mild symptoms, such as fever, rash, and muscle aches, but, in rare cases, patients can develop Guillain-Barré syndrome, a condition that drives immune cells to attack the nerves. Furthermore, infection with Zika during pregnancy can lead to debilitating birth defects, including microcephaly, in which the head and brain are abnormally small.

portrait of Marcia Castro
Marcia Castro
 

Bonds and his colleagues recently published a modeling study suggesting that in a worst-case scenario, 1.3 billion more people would live in temperature conditions suitable for Zika transmission by 2050. That scenario assumes that fossil fuels will be burned at ever-increasing rates. “It’s amazing how fast Zika takes off when temperatures are suitable for the mosquito vector,” says Bonds, who has doctoral degrees in ecology and economics. “Our models show it spreading like wildfire.” Bonds predicts that people living in most of the southern United States will over time face higher risks not only for infection by the Zika virus, but for infections by related flaviviruses in the same genus, including those that cause West Nile, dengue, and yellow fever.

Unwelcome uptick

Meanwhile, the incidence of diseases carried by an entirely different sort of vector—ticks—is exploding across the United States. According to Beard at the CDC, the number of cases of Lyme disease in the United States reported annually to the CDC recently approached 40,000. But busy doctors and public health workers often don’t have time to report Lyme disease cases, Beard says, so the real number is likely higher.

That likelihood seems feasible, based on case estimates from insurance claims data. The CDC estimates the average number of Lyme cases diagnosed and treated in the United States at 476,000 per year between 2010 and 2018, a substantial increase over the annual average of 329,000 cases documented in insurance claims between 2005 and 2010. The rise in numbers parallels corresponding increases in the geographical distribution of ticks that carry Lyme and other diseases. Tick populations are moving steadily north, and species appearing in different parts of the country are also changing.

“In the past twenty-five years,” says Beard, “the number of counties in which the blacklegged tick, which transmits the Lyme pathogen, Borrelia burgdorferi, has become established has more than doubled. The lone star tick, a vector for ehrlichiosis that was once limited largely to the southern United States, is now found all the way up into New England.”

Research indicates that many factors other than climate affect how ticks spread and come into contact with people. For instance, ticks prefer forest habitats, which in the United States have grown back following the steady decline in land cleared for agriculture since the 1800s. Thanks to conservation laws, white-tailed deer populations, which are reservoirs for ticks in the wild, have rebounded from about half a million in the early 1900s to more than 25 million today.

Human activities that influence disease risk are also changing. As suburban sprawl continues unabated, more people are spending time outdoors, where they face higher risk of infection. Beard agrees that climate change explains in part why ticks are spreading northward, but in other parts of the country, land use and human behavior play greater roles.

The human variable

Telford, who specializes in the ecology and epidemiology of tick-borne illnesses, also thinks humans play a significant role in disease risk. In a recent expert opinion in a book on climate, ticks, and disease published by CABI, an international organization dedicated to applying scientific expertise to problems affecting agriculture, Telford wrote that “human aspects of transmission risk are still poorly studied and need to be considered in any discussion of the role of climate change on vector-borne infections.” Cases of dengue fever in Mexico, he says, outnumber those in nearby parts of Texas “because Americans are more likely to have air-conditioning and stay inside, even though the mosquito habitat and breeding are identical on either side of the border.”

“The math is a lot more complicated than simply putting in a climate variable and then assuming it’s going to lead to a doubling or tripling of cases of a disease like malaria.”

Echoing points raised by Relman at Stanford, Telford speculates that climate change may not in fact generate net increases in vector-borne disease rates, assuming that rising cases in some areas are matched by declines in others. “You wind up with a shifting of the risk of disease,” Telford says. “The cases overall balance out.”

Still, social determinants and climate change can conspire to drive disease patterns in unexpected ways. Hotez cites a notable example: unprecedented temperatures of up to 50°C in the Middle East are fueling droughts that affect ancient agricultural lands, driving people to the cities, where crowding and urbanization, together with political instability, can lead to conditions that affect the rates of illness. In Aleppo, Syria, conflict has undermined infrastructure, resulting in, among other things, uncollected garbage that provides a breeding ground for sandflies that transmit a disfiguring illness called cutaneous leishmaniasis. The illness is becoming more widespread in the region.

Land-use changes can elevate disease risk by altering susceptibility to mosquito breeding, as shown by how deforestation in the Brazilian Amazon contributes to increases in malaria. Also, as new cities emerge in the Amazon, so do areas affected by dengue.

Castro does much of her field work in the Amazon, where her research focuses on mosquito-borne diseases. She says that climate change has the potential to expand areas suitable for the presence of mosquitoes and contribute to what she says are intensifying disease risks, which in many places are characterized by more frequent disease outbreaks.

“The math is a lot more complicated than simply putting in a climate variable and then assuming it’s going to lead to a doubling or tripling of cases of a disease like malaria,” Castro says. “When trying to simulate a future in which the climate is changing, you have to account for the underlying local context and epidemiology.”

Meanwhile, back in Massachusetts, Basu says clinicians need to be ready for surprising diagnoses and infectious diseases they might not otherwise expect to see. His West Nile patient eventually recovered but only after a long slog that took the better part of a year. “I tell my medical students that we need to keep monitoring and understanding the implications of global warming on our own practices. This is a dynamic process and things are changing.”

People who drink moderate amounts of coffee each day have a lower risk of death from disease


Image: People who drink moderate amounts of coffee each day have a lower risk of death from disease

Many people drink coffee for an energy boost, but do you know that it can also prolong your life? A study published in the journal Circulation revealed that moderate amounts — or less than five cups — of coffee each day can lower your risk of death from many diseases, such as cardiovascular disease, Type 2 diabetes, and nervous system disorders. It can also lower death risk due to suicide.

The study’s researchers explained this effect could be attributed to coffee’s naturally occurring chemical compounds. These bioactive compounds reduce insulin resistance and systematic inflammation, which might be responsible for the association between coffee and mortality. (Related: Coffee drinkers have a lower mortality rate and lower risk of various cancers.)

The researchers reached this conclusion after analyzing the coffee consumption every four years of participants from three large studies: 74,890 women in the Nurses’ Health Study; 93,054 women in the Nurses’ Health Study 2; and 40,557 men in the Health Professionals Follow-up Study. They did this by using validated food questionnaires. During the follow-up period of up to 30 years, 19,524 women and 12,432 men died from different causes.

They found that people who often consumed coffee tend to smoke cigarettes and drink alcohol. To differentiate the effects of coffee from smoking, they carried out their analysis again among non-smokers. Through this, the protective benefits of coffee on deaths became even more apparent.

With these findings, the researchers suggested that regular intake of coffee could be included as part of a healthy, balanced diet. However, pregnant women and children should consider the potential high intake of caffeine from coffee or other drinks.

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Because the study was not designed to show a direct cause and effect relationship between coffee consumption and dying from illness, the researchers noted that the findings should be interpreted with caution. Still, this study contributes to the claim that moderate consumption of coffee offers health benefits.

The many benefits of coffee

Many studies have shown that drinking a cup of coffee provides health benefits. Here are some of them:

  • Coffee helps prevent diabetes: A study conducted by University of California, Los Angeles (UCLA) researchers showed that drinking coffee helps prevent Type 2 diabetes by increasing levels of the protein sex hormone-binding globulin (SHBG), which regulates hormones that influence the development of Type 2 diabetes. Researchers from Harvard School of Public Health (HSPH) also found that increased coffee intake may lower Type 2 diabetes risk.
  • Coffee protects against Parkinson’s disease: Studies have shown that consuming more coffee and caffeine may significantly lower the risk of Parkinson’s disease. It has also been reported that the caffeine content of coffee may help control movement in people with Parkinson’s disease.
  • Coffee keeps the liver healthy: Coffee has some protective effects on the liver. Studies have shown that regular intake of coffee can protect against liver diseases, such as primary sclerosing cholangitis (PSC) and cirrhosis of the liver, especially alcoholic cirrhosis. Drinking decaffeinated coffee also decreases liver enzyme levels. Research has also shown that coffee may help ward off cancer. A study by Italian researchers revealed that coffee intake cuts the risk of liver cancer by up to 40 percent. Moreover, some of the results indicate that drinking three cups of coffee a day may reduce liver cancer risk by more than 50 percent.
  • Coffee prevents heart disease: A study conducted by Beth Israel Deaconess Medical Center (BIDMC) and HSPC researchers showed that moderate coffee intake, or two European cups, each day prevents heart failure. Drinking four European cups a day can lower heart failure risk by 11 percent.

Scientists Want to Align Your Internal Clock Because Timing Is Everything


internal clock

In life, timing is everything.

Your body’s internal clock — the circadian rhythm — regulates an enormous variety of processes: when you sleep and wake, when you’re hungry, when you’re most productive. Given its palpable effect on so much of our lives, it’s not surprising that it has an enormous impact on our health as well. Researchers have linked circadian health to the risk of diabetes, cardiovascular disease, and neurodegeneration. It’s also known that the timing of meals and medicines can influence how they’re metabolized.

The ability to measure one’s internal clock is vital to improving health and personalizing medicine. It could be used to predict who is at risk for disease and track recovery from injuries. It can also be used to time the delivery of chemotherapy and blood pressure and other drugs so that they have the optimum effect at lower doses, minimizing the risk of side effects.

However, reading one’s internal clock precisely enough remains a major challenge in sleep and circadian health. The current approach requires taking hourly samples of blood melatonin — the hormone that controls sleep — during day and night, which is expensive and extremely burdensome for the patient. This makes it impossible to incorporate into routine clinical evaluations.

My colleagues and I wanted to obtain precise measurements of internal time without the need for burdensome serial sampling. I’m a computational biologist with a passion for using mathematical and computational algorithms to make sense of complex data. My collaborators, Phyllis Zee and Ravi Allada, are world-renowned experts in sleep medicine and circadian biology. Working together, we designed a simple blood test to read a person’s internal clock.

Listening to the Music of Cells

The circadian rhythm is present in every single cell of your body, guided by the central clock that resides in the suprachiasmatic nucleus region of the brain. Like the secondary clocks in an old factory, these so-called “peripheral” clocks are synchronized to the master clock in your brain, but also tick forward on their owneven in petri dishes!

Your cells keep time through a network of core clock genes that interact in a feedback loop: When one gene turns on, its activity causes another molecule to turn it back down, and this competition results in an ebb and flow of gene activation within a 24-hour cycle. These genes in turn regulate the activity of other genes, which also oscillate over the course of the day. This mechanism of periodic gene activation orchestrates biological processes across cells and tissues, allowing them to take place in synchrony at specific times of day.

The circadian rhythm orchestrates many biological processes, including digestion, immune function, and blood pressure, all of which rise and fall at specific times of the day. Misregulation of the circadian rhythm can have adverse effects on metabolism, cognitive function, and cardiovascular health.
The circadian rhythm orchestrates many biological processes, including digestion, immune function, and blood pressure, all of which rise and fall at specific times of the day. Misregulation of the circadian rhythm can have adverse effects on metabolism, cognitive function, and cardiovascular health.

The discovery of the core clock genes is so fundamental to our understanding of how biological functions are orchestrated that it was recognized by the Nobel Committee last year. Jeffrey C. Hall, Michael Rosbash, and Michael W. Young together won the 2017 Nobel Prize in Physiology or Medicine “for their discoveries of molecular mechanisms controlling the circadian rhythm.” Other researchers have noted that as many as 40 percent of all other genes respond to the circadian rhythm, changing their activity over the course of the day as well.

This gave us an idea: Perhaps we could use the activity levels of a set of genes in the blood to deduce a person’s internal time — the time your body thinks it is, regardless of what the clock on the wall says. Many of us have had the experience of feeling “out of sync” with our environments — of feeling like it’s 5:00 a.m. even though our alarm insists it’s already 7:00 a.m. That can be a result of our activities being out of sync with our internal clock — the clock on the wall isn’t always a good indication of what time it is for you personally. Knowing what a profound impact one’s internal clock can have on biology and health, we were inspired to try to gauge gene activity to measure the precise internal time in an individual’s body. We developed TimeSignature: a sophisticated computational algorithm that could measure a person’s internal clock from gene expression using two simple blood draws.

Designing a Robust Test

To achieve our goals, TimeSignature had to be easy (measuring a minimal number of genes in just a couple blood draws), highly accurate, and — most importantly — robust. That is, it should provide just as accurate a measure of your intrinsic physiological time regardless of whether you’d gotten a good night’s sleep, recently returned from an overseas vacation, or were up all night with a new baby. And it needed to work not just in our labs but in labs across the country and around the world.

A mismatch between our internal time and our daily activities may raise the risk of disease.
A mismatch between our internal time and our daily activities may raise the risk of disease.

To develop the gene signature biomarker, we collected tens of thousands of measurements every two hours from a group of healthy adult volunteers. These measurements indicated how active each gene was in the blood of each person during the course of the day. We also used published data from three other studies that had collected similar measurements. We then developed a new machine learning algorithm, called TimeSignature, that could computationally search through this data to pull out a small set of biomarkers that would reveal the time of day. A set of 41 genes was identified as being the best markers.

Surprisingly, not all the TimeSignature genes are part of the known “core clock” circuit — many of them are genes for other biological functions, such as your immune system, that are driven by the clock to fluctuate over the day. This underscores how important circadian control is — its effect on other biological processes is so strong that we can use those processes to monitor the clock!

Using data from a small subset of the patients from one of the public studies, we trained the TimeSignature machine to predict the time of day based on the activity of those 41 genes. (Data from the other patients was kept separate for testing our method.) Based on the training data, TimeSignature was able to “learn” how different patterns of gene activity correlate with different times of day. Having learned those patterns, TimeSignature can then analyze the activity of these genes in combination to work out the time that your body thinks it is. For example, although it might be 7 a.m. outside, the gene activity in your blood might correspond to the 5 a.m. pattern, indicating that it’s still 5 a.m. in your body.

Many genes peak in activity at different times of day. This set of 41 genes, each shown as a different color, shows a robust wave of circadian expression. By monitoring the level of each gene relative to the others, the TimeSignature algorithm learns to ‘read’ your body’s internal clock.
Many genes peak in activity at different times of day. This set of 41 genes, each shown as a different color, shows a robust wave of circadian expression. By monitoring the level of each gene relative to the others, the TimeSignature algorithm learns to ‘read’ your body’s internal clock. 

We then tested our TimeSignature algorithm by applying it to the remaining data, and demonstrated that it was highly accurate: We were able to deduce a person’s internal time to within 1.5 hours. We also demonstrated our algorithm works on data collected in different labs around the world, suggesting it could be easily adopted. We were also able to demonstrate that our TimeSignature test could detect a person’s intrinsic circadian rhythm with high accuracy, even if they were sleep-deprived or jet-lagged.

Harmonizing Health With TimeSignature

By making circadian rhythms easy to measure, TimeSignature opens up a wide range of possibilities for integrating time into personalized medicine. Although the importance of circadian rhythms to health has been noted, we have really only scratched the surface when it comes to understanding how they work. With TimeSignature, researchers can now easily include highly accurate measures of internal time in their studies, incorporating this vital measurement using just two simple blood draws. TimeSignature enables scientists to investigate how the physiological clock impacts the risk of various diseases, the efficacy of new drugs, the best times to study or exercise, and more.

Of course, there’s still a lot of work to be done. While we know that circadian misalignment is a risk factor for disease, we don’t yet know how much misalignment is bad for you. TimeSignature enables further research to quantify the precise relationships between circadian rhythms and disease. By comparing the TimeSignatures of people with and without disease, we can investigate how a disrupted clock correlates with disease and predict who is at risk.

Down the road, we envision that TimeSignature will make its way into your doctor’s office, where your circadian health could be monitored just as quickly, easily, and accurately as a cholesterol test. Many drugs, for example, have optimal times for dosing, but the best time for you to take your blood pressure medicine or chemotherapy may differ from somebody else.

Previously, there was no clinically feasible way to measure this, but TimeSignature makes it possible for your doctor to do a simple blood test, analyze the activity of 41 genes, and recommend the time that would give you the most effective benefits. We also know that circadian misalignment — when your body’s clock is out of sync with the external time — is a treatable risk factor for cognitive decline; with TimeSignature, we could predict who is at risk, and potentially intervene to align their clocks.

The 25 Biggest Scientific Breakthroughs of 2017


Every week in 2017 seemed to bring new, objectively bad news about environmental degradation, government officials being awful, or video gamesbeing ruined by microtransactions. But it wasn’t all bad news: Very exciting and groundbreaking research was added to the scientific literature this year, reminding us that not everything is moving backward.

The 25 studies below, representing the biggest breakthroughs of the year, represent a wide and eclectic range of research areas. Let these snippets from Inverse’s interviews with researchers offer a sense of just how many scientific fields strode forward in 2017:

  • “It’s a terrible way to define different populations,” a geneticist studying skin color said.
  • “Best-case scenario, some of the advertising is true. Worst-case scenario: very little to none of the advertising is true and people may actually get hurt,” said a psychologist about the problems with mindfulness.
  • “What we showed is that diarrhea is actually really good for you,” said a scientist researching diarrhea.

Without further ado, here are the studies that rocked the science world this year, presented in order of popularity among our readers, though not necessarily importance:

25. Neanderthals Never Would Have Outlived Us

Humans still contain a small percentage of Neanderthal DNA. Even though we know that humans and Neanderthals overlapped for about 15,000 years, scientists aren’t sure how our ancient cousins died out. They’re pretty sure that Neanderthals would have been replaced by humans no matter what. Computer modeling shows that humans migrating out of Africa would have replaced Neanderthals, whether or not they died out from other factors. But while they lived together, Neanderthals left their genetic legacy imprinted in our DNA.

24. Magic Mushrooms Can Help with Depression

Scientists put tripping patients into fMRI machines to observe what their brains did under the influence of psilocybin, the active ingredient in hallucinogenic, “magic,” mushrooms. They found that patients with depression described feeling “reset” after a trip, and brain scans supported this conclusion. Patients who reported feeling better also showed reduced blood flow to parts of the brain associated with depressive symptoms.

23. Teeth From 9.7 Million Years Ago Could Rewrite Human History

Scientists found teeth in Germany that they suspect come from hominins. They date back to before similar human ancestors arose in Africa, suggesting that we may need to rework the entire human evolutionary timeline. Whether it’s a product of convergent evolution or simply related species, these fossils raise more questions about human origins than they answer.

22. Eating Weed and Spicy Food Is Good for Your Gut

More good news from 2017! Researchers found that marijuana and spicy food can ease inflammation in your digestive system, potentially paving the way for new treatments for Type 1 diabetes, colitis, and other gut issues. Capsaicin, the spicy stuff in chili peppers, makes your digestive system produce a type of cannabinoid that can offer protective benefits to your gastrointestinal tract, suggesting that edible marijuana could do the same thing. This is good news for lovers of spicy food and edibles.

21. Dogs Are Genetically Predisposed to Being Good Boys

It’s not all bad news for 2017: Scientists examining dog genetics found that dog genes predispose them to domestication and prosocial behavior. This study is the first to show why, on a molecular level, dogs are _so good). Interestingly, the scientists also found that the same genetic changes that led to domestication also seems to have made dogs less intelligent than wolves.

20. You’re More Likely to View Atheists as Serial Killers

Even though atheism has become more common in modern society, it turns out believing in something might make you seem less like a psychopath, according to a study published this year. People are more likely to believe that a killer in a hypothetical scenario is an atheist instead of a person of faith, according to research published this year. This finding even held true for atheists, perhaps suggesting some internalized stigma leading to unconscious bias. Even Mark Zuckerberg has taken note of this anti-atheist prejudice, announcing his faith a year ago.

19. Human-Pig Chimeras Have a “Safety Switch”

Scientists shocked the world when they announced they’d developed a human-pig chimera, bringing us a step closer to growing human organs inside pigs. But they also soothed our fears of a pig-man apocalypse when they assured us that there is a self-destruct mechanism for human stem cells that accidentally travel to the pig brains. It’s not even clear whether that would lead to enhanced consciousness, but if this safety switch works, we won’t have to worry about it.

18. Psychologists are Growing Skeptical of Mindfulness Practices

Mindfulness has become a pop psychology buzzword recently, and psychology professionals are concerned. Fifteen psychologists published a paper this year outlining their concerns that corporate seminars, meditation workshops, and the like are offering psychological benefits that are unproven while ignoring risks. After all, psychological health is not one-size-fits-all.

17. Even Occasional Drinks Can Affect Your Brain Health

We all know that drinking too much can cause chronic health problems, but a massive cohort study of British civil servants found that moderate drinking accelerates cognitive decline. Over 30 years of surveys and health check-ups, the participants who consumed 14 to 21 units of alcohol per week “had three times the odds of right sided hippocampal atrophy,” an early warning sign of Alzheimer’s disease. This is a serious buzzkill, since previous research has suggested that moderate drinking could have certain benefits for heart health. Following this cohort of research subjects further will reveal more about their health as they age.

16. Your Face Shows Signs of Class Boundaries

It’s sometimes easy to tell whether someone is wealthy based on their clothes, car, home, and other material things. But this year researchers found that social status may show in your face, too. This doesn’t mean that some people are genetically predisposed to be rich, but rather that being poor can impart subtle, lifelong mood symptoms that observers can see on your face even when you’re wearing a neutral expression. Worryingly, the researchers found that this judgment can impair hireability, which could perpetuate class boundaries.

15. Scientists Identified the Maximum Human Lifespan

Life extension advocates like to say that, with the right supplements and therapies, you’ll be able to live long enough to see science bring about immortality. But more conventional-thinking researchers say this isn’t so. They identified the maximum human lifespan as 115.7 years for women and 114.1 years for men. This area of research is still hotly debated, but the new findings fit pretty closely to what other groups have said.

14. A Supervolcano Could Go Off Way Sooner Than We Think

As if 2017 wasn’t bad enough, statisticians say we’re overdue for a supervolcano eruption. On the basis of geological records, a team of researchers estimated that cataclysmic supervolcano eruptions on Earth occur, on average, every 17,000 years. The last one happened 20 to 30 thousand years ago. You do the math.

13. Geneticists Discovered That Light Skin Variations Originated in Africa

Science has often been used in the service of justifying racism, but scientists shut down outdated notions of genetic differences among humans of different ethnic groups this year. Geneticists found that variants associated with light skin actually originated in Africa, not only disproving the backward notion that people with darker skin are less human, but also calling into question the notion that skin color can be associated with certain ethnic groups.

12. Scientists Find the Oldest Human Skeleton in the Americas

After re-examining a skeleton stolen from a submerged cave in Mexico, scientists determined that it may represent the oldest human remains ever found in the Americas. At 13,000 years old, the 80-percent-complete skeleton suggests that humans came to the Americas thousands of years before the people that were previously thought to be the first Americans.

11. Diarrhea Is Your Body’s Immune System Savior

Diarrhea sucks, but there’s actually a good reason for it. Mice infected with a mouse bacteria similar to E. coli exhibited changes in intestinal cells in a way that seemed to cause diarrhea. Scientists have long suspected that diarrhea was the body’s way of clearing out disease, but this study provided the first solid proof.

10. Redditors’ Dicks Match Up With Dick Size Desires

Many penis-havers worry about whether their penis size will match up with the preferences of penis-likers. In a study conducted by and among redditors, they found that penis sizes matched up pretty well with what their potential partners want. These findings fit with what academic researchers have found, but maybe this citizen science confirmation will be more digestible for redditors.

9. Porn Can Change Your Brain

People who watch a lot of pornography don’t necessarily have an addiction or a psychological condition. But neuroscientists have found that people who struggle with their porn use exhibit brain changes. They react more strongly to reward cues associated with porn, similar in some ways to gambling addicts. It’s not clear whether porn addiction is a real condition, though.

8. Scientists Send Data to and from Space Using Quantum Entanglement

Scientists in China transmitted a quantum state almost a thousand miles into space, much farther than had been done previously. This development brought scientists one step closer to the kind of technology that could enable quantum computing. Quantum entanglement is a burgeoning topic in physics that even Albert Einstein didn’t believe could exist.

7. Human Mini-Brain Organoids Raise Ethical Concerns

Scientists can grow miniature models of human organs, called organoids that allow them to perform research that would be unethical on living. But when scientists reported that human brain organoids grafted onto rat brains had begun to integrate, this raised ethical red flags. If a rat has a partially human brain, should we be doing science on it that we wouldn’t do on a human?

Alex Jones

6. Conspiracy Theorists Think Differently

European social psychologists have shed some light on what makes the nearly half of American conspiracy theorists different from the rest. They exhibit a phenomenon called illusory pattern perception, which makes them see patterns of danger where there is no danger. This is the first scientific evidence linking illusory pattern perception to belief in conspiracy theories.

5. Ancient Humans Knew How to Avoid Incest

We know that incest increases the chances of developing genetic diseases, but it turns out our early human ancestors knew about the risks of incest, too. Geneticists and archaeologists examining 34,000-year-old human remains from Russia found that four people buried together were no closer than second cousins, suggesting that even ancient humans made efforts to avoid inbreeding. Researchers say this probably means these early humans made a purposeful effort to mix outside their family groups, including some semblance of romance, as indicated by the jewelry included in their collective burial.

4. Scientists Discovered Our Black Hole Neighbors

Astronomers using NASA’s NuSTAR X-ray telescope found evidence of two super-massive black holes. At the center of galaxies near the Milky Way, they’re still millions of light-years away, but in relative terms, they’re our next-door neighbors.

3. Long-Term Marijuana Use Changes Your Brain

Marijuana is safe, as far as drugs go, but that doesn’t mean it’s totally free of long-term consequences. In a mouse study, neuroscientists found that long-term marijuana use can lead to abnormally high dopamine levels. This suggests that marijuana could be messing with your brain chemistry more than you thought.

2. Scientists Figured Out That Tattoo Ink Doesn’t Stay Put

That’s right, even though the whole idea of a tattoo is that the ink goes into your skin and never comes out, researchers have found that ink pigment nanoparticles migrate and accumulate in people’s lymph nodes. It makes sense since your lymphatic system gets rid of bad stuff and tattoo ink is essentially a foreign invader.

Forever Young: 14 Reasons Why People 100 Years Ago Died So Much Younger Than We Do Now.


list of diseases

These 14 diseases have largely been eradicated or at least significantly decreased in the U.S. due to vaccinations. 

It’s common knowledge that back in the day, humans didn’t live as long as we do now. In fact, an average person’s life expectancy has risen from around 48 years in the early 1900s to well over 70 now. In Japan, the average life expectancy is 83.

In addition to improved sanitation and overall better hygiene — medical advancements, antibiotics, and of course, vaccines have all aided in expanding our life spans. Before vaccines were developed, there were a handful of fatal, debilitating diseases that threatened to kill us well before we reached ripe old age; they’re depicted in the infographic below.

 

Thank goodness for vaccines, right? Polio, a debilitating disease that causes paralysis and death in children, has fortunately been wiped out completely in most countries except for a handful.

As a result of fear-mongering, however, vaccine rates in the U.S. have dropped in recent years — causing an increase in diseases that were once thought to be gone for good. For example, measles has made a comeback in New York City, where 19 cases were confirmed this year — and occurred in people who weren’t vaccinated. If you’re one of those who weren’t vaccinated, perhaps it’s time to think about getting a measles shot: “If you are unvaccinated and you come in contact with measles, there’s a 90% chance you will get it,” Jason McDonald, a spokesperson for the Centers for Disease Control and Prevention (CDC) said.

Other diseases – such as mumps, whooping cough, and chicken pox, have also sprouted up in recent years, often due to a wave of celebrities and parents voicing their beliefs that vaccines cause autism and are full of toxins. According to the CDC and various studies completed in recent years, however, vaccines are entirely safe and quite essential in providing a healthy life for your children. View this map to see how vaccine-preventable outbreaks have occurred across the world since 2008.

And if we decide to let vaccine scares take over the country? Cases of more diseases might flare up again, as depicted by the infographic below. So don’t be afraid of vaccines; rather, be afraid of the diseases they prevent — which were capable of killing our ancestors far more easily and quickly.

What Could Happen if we Stop Vaccinating?