Browse evidence-based analysis of health-related claims and assertions
A genetic glitch in one inhibitory receptor (FcγRIIB) stops it from working properly, so the immune system can’t calm down — leading to attacks on the body’s own tissues.
Mechanistic
When immune cells grab antibody-tagged germs, they turn on signals (like CD86 and CD40) and release alarm chemicals (like IL-6 and TNF-α) that tell T cells to wake up and fight.
A special receptor (FcRn) saves antibodies from being destroyed inside cells and helps shuttle them — along with any germs they’re attached to — to the right place to be shown to immune cells.
One type of receptor (FcγRIIB) can also swallow antibody-tagged germs, but it doesn’t turn on the immune system as strongly — it needs 30 times more germs to get the same effect as the activating receptors.
Quantitative
When antibodies tag a germ, immune cells that show antigens to killer T cells do a much better job of it than if the germ was just floating around without tags.
When antibodies stick to germs and bind to certain receptors on immune cells, the cell swallows the whole thing into a bag that goes to a trash compactor (lysosome) to break it down for display.
One type of receptor (FcγRI) grabs onto single antibodies really tightly, while other receptors only grab well when many antibodies are stuck together on a germ.
Descriptive
Certain receptors on immune cells grab onto antibodies attached to germs, helping the cells swallow them up so they can be broken down and shown to other immune cells.
When tested in animals at high doses, natural and man-made chemicals are about equally likely to show up as cancer-causing.
The 27 plant chemicals that caused cancer in rats at high doses are also found in everyday foods like fruits and vegetables.
Out of the 52 plant-made pesticides tested in animals, 27 caused cancer in rodents when given very high doses.
Scientists have tested 52 plant-made pesticides in very high doses on animals to see if they cause cancer.
Almost all the pesticide-like chemicals we eat in our food come from plants themselves, not from man-made products.
From 2000 to 2006, both 'bad' and 'good' cholesterol levels in heart disease patients admitted to the hospital gradually went down.
Women with heart disease tend to have higher 'bad' cholesterol levels when they’re admitted to the hospital than men do.
Correlational
Very few heart disease patients—just 1 in 70—have both very low 'bad' cholesterol and high 'good' cholesterol at the time they’re admitted to the hospital.
More than half of heart disease patients admitted to the hospital have low levels of 'good' cholesterol, which is linked to higher heart disease risk.
When people with heart disease are admitted to the hospital, their 'bad' cholesterol is usually around 105 mg/dL, which is higher than what doctors now recommend for heart health.
If you’re already strong and trained, you don’t need fancy workout tricks like pyramids or going to failure to get the best results—just do the same total work with any method.
Causal
The researchers made sure everyone did the exact same total amount of work—same number of reps, same weights—so any differences in results could only be because of how they did the workout, not how much they lifted.
By having each person train one leg one way and the other leg another way, the study made sure that differences in people’s bodies didn’t mess up the results—so we can be sure it’s the training method, not the person, that matters.
Going from light to heavy and back to light again in your workouts doesn’t make you stronger or bigger than just doing the same total weight with consistent loads—if you’re already trained.
Even if you push yourself to complete exhaustion with drop sets, you won’t grow bigger or stronger than if you just stick to regular sets—as long as you lift the same total weight.
If you lift the same total weight no matter how you arrange your sets—pyramid, failure, or regular—you’ll get the same results. Fancy methods don’t make you stronger or bigger if you’re already trained.