You may not exactly like the things you learn about fat in today’s post, but fat seems to be society’s public enemy number one lately, and you know what they say — it’s always best to know your enemy.

Here’s a fat cell:

It’s relatively huge as far as cells go. With a diameter of about a tenth of a millimeter, it’s over 100 times the size of a skin cell, and just one fat cell is potentially visible by the naked eye. As you can see, most of a fat cell is a huge pool of fat, with all of the other parts of the cell squished off to the side. If you’re the average adult, you’ve got about 30 billion of these guys. All the more reason to know what they’re capable of, right?

1. Fat cells can pilfer your medications and vitamins. At the most basic level, when you take medicine or vitamins, your body uses what you need and the byproducts or whatever your body doesn’t use are excreted. However, many vitamins (like A, D, E, and K) and medications (including many antidepressants and anesthetics) are fat-soluble, as opposed to water-soluble, meaning that as they circulate your body they can slip out of your blood and into your fat. THC, the active compound in marijuana, is an example of a fat-soluble drug; if an obese person with large amounts of body fat gets high with a skinny person with low levels of body fat, it is likely that the obese person would test positive for a longer stretch of time, because the obese person has more fat cells to trap the THC and release its metabolites more slowly over time.

Sneaky fat cells…

2. Fat cells influence how hungry you are and whether or not you get diabetes and heart disease. As it turns out, fat cells don’t just take stuff out of your blood, they put stuff in it, too. In particular, fat cells make a whole bunch of hormones and inflammatory molecules. One of the most important molecules made by fat is leptin, which signals to the brain and decreases appetite. Mice without receptors for leptin become obese:

Fat tissue also releases inflammatory molecules called cytokines that can decrease the ability of the body to respond to insulin, which can set the stage for diabetes. Some of these inflammatory molecules are also thought to promote systemic inflammation, and research suggests that this can make atherosclerosis (artery blockage due to fat accumulation) all the more dangerous. That’s because inflammatory cells might be able to rupture atherosclerotic buildup, creating clots that induce heart attacks or strokes.

This is a lot of information to take in, and the many roles of fat as a signaling tissue make up a very active area of research right now, especially because fat can often turn on or off production of specific molecules in obese individuals.

3. Fat cells can feed cancer cells. If you weren’t hating fat by now, this might just tip the scales. Very recent research in Nature Medicine suggests that abdominal cancers, like ovarian cancer, are made worse by fat. Ovarian cancers tend to metastasize to fat-dense regions of the abdomen, and fat cells can directly transfer fat to cancer cells, which provides the cancer with energy and allows it to grow in size.The silver lining of these findings is that researchers may now have a new mechanism to target when designing drugs to fight cancers that flourish in fatty areas of the body.

4. Fat cells might be the cure to just about everything. Alright, last but not least, a major redeeming feature of fat: it’s got stem cells in it. In general, stem cells are cells that have the potential to differentiate into multiple other cell types. Scientists have theorized stem cells to be a potential therapy for just about every disease condition (e.g. using stem cell-derived neurons to replace the lost/damaged neurons in neurodegenerative diseases). Although fat stem cells can’t turn into as many cell types as embryonic stem cells can, they have many upsides: fat stem cells circumvent ethical concerns, are readily available thanks to all of the fat-removing surgeries done today, and pose far less risk of immune rejection when re-introducing cells taken from someone’s own fat. Fat stem cells have already been shown to essentially cure a mouse model of lupus.

So maybe you’re not necessarily any happier about your fat now, but I hope you have a new appreciation for it. While you lament your muffin top, you can consider the diverse biology of your muffin top. That might sound nerdy, but…well, that’s the whole point.

Ovchinnikova O, Robertson AK, Wågsäter D, Folco EJ, Hyry M, Myllyharju J, Eriksson P, Libby P, & Hansson GK (2009). T-cell activation leads to reduced collagen maturation in atherosclerotic plaques of Apoe(-/-) mice. The American journal of pathology, 174 (2), 693-700 PMID: 19131590

Nieman KM, Kenny HA, Penicka CV, Ladanyi A, Buell-Gutbrod R, Zillhardt MR, Romero IL, Carey MS, Mills GB, Hotamisligil GS, Yamada SD, Peter ME, Gwin K, & Lengyel E (2011). Adipocytes promote ovarian cancer metastasis and provide energy for rapid tumor growth. Nature medicine, 17 (11), 1498-503 PMID: 22037646

Choi EW, Shin IS, Park SY, Park JH, Kim JS, Yoon EJ, Kang SK, Ra JC, & Hong SH (2011). Reversal of serological, immunological and histological dysfunction in systemic lupus erythematosus mice by long-term serial adipose tissue-derived mesenchymal stem cell transplantation. Arthritis and rheumatism PMID: 21904997

Bowed femurs in a 2-year-old with rickets.

Now that I’m back from visiting amusement parks in Orlando, FL, I think it’s as good a time as any to reveal a little secret of mine: I don’t wear sunscreen. (“Not even in Florida?!”) Not even in Florida. In August.

I want to be really emphatic in saying that I am NOT advocating for people to go without sunscreen. You have to do what works for you. I was raised in sunny places and I almost never get sunburns, and now that I live in New England I’m much more likely to get frostbite than a sunburn anyway. Ultimately, I don’t do much stuff outside, so when I do, I don’t want anything coming between me and my sun.

But for all you sunscreen users, I do want to advocate “everything in moderation.” As it turns out, excessive sunscreen use is being blamed at least in part for the recent worldwide increase in rickets. (“Rickets? As in that disease that pirates used to get along with scurvy and scabies?”) Yes, that rickets. Read on for more on how sunscreen might save your skin, but bend your bones.

When I was a kid, I seem to remember most sunscreens being SPF 30. And maybe most of them still are, but I feel like I’ve noticed some brands entertaining the idea of “the more SPF, the better.” Namely, Neutrogena sells an “Age Shield” lotion with an unbelievably high SPF of 110. What is SPF? Well, the FDA calculates it from a complicated formula:

But consumers can think of it as an indication of the amount of protection provided against UV-B, the ultraviolet rays that cause sunburn. Given that an SPF of 15 blocks 94% of UV-B rays and an SPF of 45 blocks 98%…what exactly is SPF 100+ doing? Well, technically, not much, because the benefits from increasing SPF really level off after SPF 45. What the incredibly high SPF sunscreens are doing, in my opinion, is feeding into the notion that sun exposure is a very, very bad thing that people should protect against at all costs.

But it’s not. You may have heard at one point or another that sunlight triggers the production of vitamin D in our skin. In fact, those same UV-B rays that people go to such lengths to block out are the same rays that turn the 7-dehydrocholesterol (a cholesterol derivative) in our skin into a precursor of vitamin D.

This is where rickets comes in. Because vitamin D helps the body absorb calcium, a deficiency in vitamin D means a deficiency in calcium, and without calcium bones can become soft, weak, and bendy. I’ve tried to sum all this up with the help of ClipArt:

A very fancy, complex scientific diagram

Sadly, rickets mostly occurs in children, whose bones are still forming. At Disney World, I saw endless amounts of sunscreen being slathered onto children by protective mothers who were probably doing the right thing, given the hours that would be spent in the harsh Florida sun. But what about the kid who’s only going to the park for 30 minutes in Chicago during the winter? He might be better off without the SPF.

While rickets has traditionally been thought of as a disease from long ago when diets were poor and pirates went on long voyages with more alcohol than vitamins, the advent of things like dietary supplements and the food pyramid have largely eradicated rickets in modern times. That’s why it’s come as a shock over the last year or so that rickets has been on the rise again in kids. One case receiving particular attention this January was that of 12-year-old U.K. girl Tyler Attrill whose mother was a nurse who never failed to put SPF 50 on her kids when they went outside. So when Tyler complained of extreme leg pain, it was a surprise to learn that the actions of a conscientious parent had contributed to the early stages of rickets in her child. Tyler became somewhat of a poster child for the broader trend of rickets symptoms in kids who are overprotected from the sun by well-meaning parents.

My point in all of this is that it could be a good thing if you forget your sunscreen every now and again. Rickets can occur in adults, so you’re never too old to benefit from some extra vitamin D for your bones. And while it’s absolutely advisable to use sunscreen to protect against skin cancer and wrinkles, don’t forget about your bones in the process. Rickets is totally preventable, so maybe for your next walk in the park you could consider trading some SPF for SWF (Sunlight Without Fear).

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Stay nerdy

P.S. I did see an okapi at Disney World! Bizarre!

Lowdon J (2011). Rickets: concerns over the worldwide increase. The journal of family health care, 21 (2), 25-9 PMID: 21678784