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The main cause for diabetes is lack of insulin in the body. Insulin is the hormone that allows body cells to absorb glucose from the blood. With out insulin, the body cells can't get glucose from the blood. So, why doesn't diabetes cause death by starvation?
Not all cells depend on insulin to take in glucose from blood (e.g. vascular endothelial cells). But the majority do (muscle tissue and fat tissue).
The lack of insulin causes the cell to use auxiliary metabolic pathways to generate its energy :
- in muscle, the protein breakdown is stimulated
- liver gluconeogenesis is stimulated by low insulin levels and high amino acid levels in blood and using substrate from muscle and fat tissue
- glucocorticoids stimulate lipolysis
- liver starts ketone body synthesis, which along with medium chain fatty acids prove to be quite a good alternative energy source for the brain
Energy from nutritional principles is as follows:
- Lipids = 9 kcal/g
- Proteins = 4 kcal/g
- Carbohydrates = 4 kcal/g - the most important because they are used as is. Lipids and proteins require energy from other sources to start chemical reactions which yield energy.
- Mark Brandt, Ph.D. Endocrine Notes Supplement from Rose Hulman Institute of Technology, pages 78-80
- Wikipedia (links)
Glucose enters your cells via a family of transporters. A primary transporter in muscle and fat cells is known as GLUT-4. Insulin stimulates GLUT-4 to move from the interior of a cell to the cell surface, where the glucose can then bind to the GLUT-4 transporter and enter the cell. However, there are plenty of glucose transporters on the cell surface, even when there is no insulin. In fact, there are enough transporters on the cell surface to allow the cell to get enough glucose to sustain its energy needs. Thus, glucose transport into cells is never truly dependent upon insulin. Insulin enhances the uptake of glucose into cells, but it is not required for it. In fact, when you knock out the insulin receptor in mice so that insulin cannot stimulate glucose uptake into muscle or fat cells (yet you keep the insulin receptor intact on other cells like brain and liver), the animals do not become diabetic and they have normal blood sugars.-https://www.ncbi.nlm.nih.gov/pubmed/15254588
Metabolic tracer studies have allowed us to learn how insulin operates in humans in vivo. When you take a type I diabetic off insulin, blood glucose climbs sharply. However, it's not because glucose can't get into cells. In fact, glucose uptake into cells actually increases. This is because the concentration of glucose in the blood is so much higher than the cellular concentration that glucose must move into the cells (remember, there's already enough glucose transporters on the cell surface even if there's no insulin). So why does blood glucose climb so high? Remember that the amount of glucose in your blood is both a function of how much glucose is entering the blood (the rate of appearance), as well as how much glucose is leaving the blood (the rate of disappearance). In a fasted diabetic without insulin, all of the glucose is coming from the liver. Remember that your liver helps maintain blood sugar levels when you are fasted by releasing glucose; this glucose comes from both gluconeogenesis (the formation of glucose from non-carbohydrate sources, like protein) and glycogenolysis (the breakdown of glycogen stored in your liver). Insulin acts as a brake (a chalone as Dr. Schafer described it) on these processes. Thus, when you do not have insulin, you have runaway gluconeogenesis and glycogenolysis. The high blood sugar in an uncontrolled diabetic is thus caused by overproduction of glucose from the liver, not because glucose can't get into cells.-http://m.bja.oxfordjournals.org/content/85/1/69.short
Polyphagia – Increased Appetite
Polyphagia is the medical term used to describe excessive hunger or increased appetite and is one of the 3 main signs of diabetes.
An increase in hunger is usually a response to normal things such as intensive exercise or other strenuous activity, but polyphagia can also be the result of more severe issues such as depression or stress.
Also known as hyperphagia , it is one of the three main symptoms of diabetes, along with:
What causes gestational diabetes?
Scientists believe gestational diabetes, a type of diabetes that develops during pregnancy, is caused by the hormonal changes of pregnancy along with genetic and lifestyle factors.
Hormones produced by the placenta contribute to insulin resistance, which occurs in all women during late pregnancy. Most pregnant women can produce enough insulin to overcome insulin resistance, but some cannot. Gestational diabetes occurs when the pancreas can’t make enough insulin.
As with type 2 diabetes, extra weight is linked to gestational diabetes. Women who are overweight or obese may already have insulin resistance when they become pregnant. Gaining too much weight during pregnancy may also be a factor.
Hormonal changes, extra weight, and family history can contribute to gestational diabetes.
Genes and family history
Having a family history of diabetes makes it more likely that a woman will develop gestational diabetes, which suggests that genes play a role. Genes may also explain why the disorder occurs more often in African Americans, American Indians, Asians, and Hispanics/Latinas.
Diabetes: 12 warning signs that appear on your skin
Diabetes can affect many parts of your body, including your skin. When diabetes affects the skin, it’s often a sign that your blood sugar (glucose) levels are too high. This could mean that:
You have undiagnosed diabetes, or pre-diabetes
Your treatment for diabetes needs to be adjusted
If you notice any of the following warning signs on your skin, it’s time to talk with your doctor.
1. Yellow, reddish, or brown patches on your skin
This skin condition often begins as small raised solid bumps that look like pimples. As it progresses, these bumps turn into patches of swollen and hard skin. The patches can be yellow, reddish, or brown.
- The surrounding skin has a shiny porcelain-like appearance
- You can see blood vessels
- The skin is itchy and painful
- The skin disease goes through cycles where it is active, inactive, and then active again
- Get tested for diabetes, if you have not been diagnosed.
- Work with your doctor to better control your diabetes.
- See a dermatologist about your skin. Necorbiosis lipodica is harmless, but it can lead to complications.
2. Darker area of skin that feels like velvet
A dark patch (or band) of velvety skin on the back of your neck, armpit, groin, or elsewhere could mean that you have too much insulin in your blood. This is often a sign of prediabetes. The medical name for this skin condition is acanthosis nigricans.
Acanthosis Nigricans (AN)
Often causing darker skin in the creases of the neck, AN may be the first sign that someone has diabetes.
3. Hard, thickening skin
When this develops on the fingers, toes, or both, the medical name for this condition is digital sclerosis.
On the hands, you’ll notice tight, waxy skin on the backs of your hands. The fingers can become stiff and difficult to move. If diabetes has been poorly controlled for years, it can feel like you have pebbles in your fingertips.
Hard, thick, and swollen-looking skin can spread, appearing on the forearms and upper arms. It can also develop on the upper back, shoulders, and neck. Sometimes, the thickening skin spreads to the face, shoulders, and chest.
In rare cases, the skin over the knees, ankles, or elbows also thickens, making it difficult to straighten your leg, point your foot, or bend your arm. Wherever it appears, the thickened skin often has the texture of an orange peel.
This skin problem usually develops in people who have complications due to diabetes or diabetes that is difficult to treat.
- Tell your doctor about the thickening skin. Getting better control of your diabetes can bring relief.
- You may also need physical therapy. When the thickening skin develops on a finger, toe, or other area with joints, physical therapy can help you keep your ability to bend and straighten the joint.
It’s rare, but people with diabetes can see blisters suddenly appear on their skin. You may see a large blister, a group of blisters, or both. The blisters tend to form on the hands, feet, legs, or forearms and look like the blisters that appear after a serious burn. Unlike the blisters that develop after a burn, these blisters are not painful.
Large blisters like this one can form on the skin of people who have diabetes.
The medical name for this condition is bullosis diabetricorum. Sometimes, it’s called diabetic bullae.
- Tell your doctor about the blisters. You’ll want to take steps to prevent an infection.
- Talk with your doctor about how to better control your diabetes.
5. Skin infections
- Hot, swollen skin that is painful
- An itchy rash and sometimes tiny blisters, dry scaly skin, or a white discharge that looks like cottage cheese
Has it been a year or longer since your last period, and do you get several yeast infections each year? It’s possible that you have diabetes or pre-diabetes.
- Get immediate treatment for the infection.
- Tell your doctor if you have frequent skin infections. You could have undiagnosed diabetes.
- If you’ve been diagnosed with diabetes, you may need better control of it.
6. Open sores and wounds
Having high blood sugar (glucose) for a long time can lead to poor circulation and nerve damage. You may have developed these if you’ve had uncontrolled (or poorly controlled) diabetes for a long time.
Poor circulation and nerve damage can make it hard for your body to heal wounds. This is especially true on the feet. These open wounds are called diabetic ulcers.
Diabetes and feet
If you have diabetes, you should check your feet every day for sores and open wounds.
- Get immediate medical care for an open sore or wound.
- Work with your doctor to better control your diabetes.
7. Shin spots
This skin condition causes spots (and sometimes lines) that create a barely noticeable depression in the skin. It’s common in people who have diabetes. The medical name is diabetic dermopathy. It usually forms on the shins. In rare cases, you’ll see it on the arms, thighs, trunk, or other areas of the body.
Diabetic dermopathy: This 55-year-old man has had diabetes for many years.
The spots are often brown and cause no symptoms. For these reasons, many people mistake them for age spots. Unlike age spots, these spots and lines usually start to fade after 18 to 24 months. Diabetic dermopathy can also stay on the skin indefinitely.
- Tell your doctor about these spots.
- Work with your doctor to better control your diabetes.
- If you haven’t been diagnosed with diabetes, get tested.
8. Outbreak of small, reddish-yellow bumps
When these bumps appear, they often look like pimples. Unlike pimples, they soon develop a yellowish color. You’ll usually find these bumps on the buttocks, thighs, crooks of the elbows, or backs of the knees. They can form anywhere though.
These bumps appear suddenly and clear promptly when diabetes is well-controlled.
When these bumps appear, they often look like pimples. Unlike pimples, they soon develop a yellowish color. You’ll usually find these bumps on the buttocks, thighs, crooks of the elbows, or backs of the knees. They can form anywhere though. No matter where they form, they are usually tender and itchy. The medical name for this skin condition is eruptive xanthomatosis.
- Tell your doctor about the bumps because this skin condition appears when you have uncontrolled diabetes.
- Talk with your doctor about how to better control your diabetes.
9. Red or skin-colored raised bumps
Whether this skin condition is associated with diabetes is controversial. We know that most people who have granuloma annulare do not have diabetes. Several studies, however, have found this skin condition in patients who have diabetes. One such study found that people with diabetes were most likely to have granuloma annulare over large areas of skin and that the bumps came and went. Another study concluded that people who have granuloma annulare that comes and goes should be tested for diabetes.
This skin condition causes bumps and patches that may be skin-colored, red, pink, or bluish purple.
- Let your doctor know if you have bumps like those shown here, especially if the bumps come and go.
10. Extremely, dry itchy skin
Dry, itchy skin
If you have diabetes, you’re more likely to have dry skin. High blood sugar (glucose) can cause this. If you have a skin infection or poor circulation, these could also contribute to dry, itchy skin.
- Tell your doctor about your extremely dry skin. Gaining better control of diabetes can reduce dryness.
- If you continue to have dry skin after you gain better control of your diabetes, a dermatologist can help.
11. Yellowish scaly patches on and around your eyelids
These develop when you have high fat levels in your blood. It can also be a sign that your diabetes is poorly controlled. The medical name for this condition is xanthelasma.
- Tell your doctor about the yellowish scaly patches around your eyes.
- Talk with your doctor about how to better control your diabetes. Controlling diabetes can clear the scaly patches.
12. Skin tags
Many people have skin tags—skin growths that hang from a stalk. While harmless, having numerous skin tags may be a sign that you have too much insulin in your blood or type 2 diabetes.
These growths are most common on the eyelids, neck, armpit, and groin.
- Ask your doctor if you should get tested for diabetes.
- If you have diabetes, ask your doctor if you need better control of it.
When to see a dermatologist
Diabetes can cause many other skin problems. Most skin problems are harmless, but even a minor one can become serious in people who have diabetes. A board-certified dermatologist can recognize skin problems due to diabetes and help you manage them.
Are all dermatologists board certified?
No. See what it takes to become board certified.
Image 1: Image Courtesy of Clark C. Otley, MD. All Rights Reserved
Images 3, 7, 8, 9: Used with permission of the American Academy of Dermatology National Library of Dermatologic Teaching Slides.
Some images used with permission of Journal of the American Academy of Dermatology
Images 5, 6 and 10: Getty Images
Cohen Sabban, EN. “Cutaneous manifestations of diabetes mellitus from A to Z.” Focus session presented at: 74th Annual Meeting of the American Academy of Dermatology March 4-8, 2016 Washington D.C.
Duff M, Demidova O, et al. “Cutaneous manifestations of diabetes mellitus.” Clinical Diabetes. 201533:40-8.
Kalus AA, Chien AJ, et al. “Diabetes mellitus and other endocrine disorders.” In: Wolff K, Goldsmith LA, et al. Fitzpatrick’s Dermatology in General Medicine (seventh edition). McGraw Hill Medical, New York, 2008:1461-70.
McKinley-Grant L, Warnick M, et al. “Cutaneous manifestations of systemic disease.” In: Kelly AP and Taylor S. Dermatology for Skin of Color. (first edition). The McGraw-Hill Companies, Inc. China, 2009:481-4.
Morgan AJ and Schwartz RA. “Diabetic dermopathy: A subtle sign with grave implications.” J Am Acad Dermatol. 200858:447-51.
Yosipovitch G, Loh KC, et al. “Medical pearl: Scleroderma-like skin changes in patients with diabetes mellitus.” J Am Acad Dermatol. 200348:109-11.
Starvation can reverse type 2 diabetes
A new study shows that starvation (eating 600 kcal/day) can reverse type 2-diabetes, just like gastric bypass surgery.
Again, there is no need to explain the effect of the surgery with other speculative theories. The resulting starvation reverses diabetes. And the starvation isn’t even necessary to do that.
If a type 2 diabetic stops eating (carbs) the symptoms of diabetes starts to go away. But starvation or surgery are unnecessarily painful ways to do it.
Luckily diabetics can eat real food to satiety, as long as they avoid sugar and starch. The food that quickly turns into simple sugars in the gut. Cutting away their stomach or starving themselves is not necessary.
All they need is good food.
A Gastric Bypass operation protects from eating too much carbohydrates in two ways. Number one: you can only eat miniature portions of anything. Number two: the smaller amounts of starch you eat is not digested as easily as the duodenum with the starch-digesting enzyme amylase is diverted from direct contact with the food.
Firstly, I agree food is the cause of diabetes two as it seems, as I understand, not a doctor, but diabetes is a dietary problem yes? Its reversible and can be put into remission or dare I use the word cure the forbidden so called word. many critics will not appreciate and fluff their feathers, but the world does not seem to grasp, that perhaps, after reading information it seems the crux of the problem the root cause of diabetes if I can quote that info is doctors have to focus target the CAUSE of diabetes and not the sugars which is only the symptom, and I can relate to this pragmatic and common sense viewing. Putting low carb and exercise aside, its seems common sense, cut down food amounts and intake with reasonableness.
Secondly, I agree 100% the video two lies about diabetes, pity the medical industry dont view the same.
Keep up the good work as long as it is done within reason and not affecting other issues.
Far from a Cure
Allen’s diet treatment was nowhere near a cure. It took patients with diabetes to the brink of starvation for the ability to work to control their disease. Many patients sought this treatment method, even though it was painful, it did help to extend their lives. This treatment method also enabled many patients to live long enough to be on the receiving end of the newly discovered insulin when it was available.
In 1918, Allen left Rockefeller to start his own treatment clinic of diabetes and metabolic disorders. After insulin was discovered, he was one of the first doctors who received samples to try on patients before it was widely distributed.
Insulin resistance in skeletal muscle
Studies using 13 C and 31 P magnetic resonance spectroscopy identified impaired insulin-stimulated glycogen synthesis as the major factor responsible for insulin resistance in muscle and reduced insulin-stimulated glucose transport activity as the rate-controlling step that underlies lower glycogen synthesis in patients with T2D and their insulin-resistant relatives 75,76,77,78,79 (Fig. 2a). Reduced insulin-stimulated glucose transport can be mainly attributed to defective insulin signalling at the level of IR and IRS-1-associated PI3K, which has been observed in one study to occur without altered AKT phosphorylation 80 . Whereas the majority of studies in humans point to proximal defects in insulin signalling, some experimental models provide evidence for distal abnormalities 81,82 . Glycogen synthase can also be stimulated via insulin regulation of glycogen synthase kinase-3 (GSK3) or independently via allosteric activation by glucose-6-phosphate 83 in skeletal muscle 75,76,77,84 and liver 38,85 , but its activity does not appear to regulate insulin-stimulated glucose disposal (Figs. 1, 2).
Lean first-degree relatives of patients with T2D present with predominantly muscle insulin resistance 76 . Ingestion of two high-carbohydrate meals revealed their early metabolic abnormalities: ingested carbohydrates were diverted from muscle glycogen synthesis to the liver, where augmented carbohydrate availability and compensatory hyperinsulinaemia promoted hepatic DNL, hepatic TAG synthesis and VLDL secretion, hypertriglyceridaemia and reduced plasma high-density lipoproteins 30 . The critical importance of skeletal muscle is illustrated by the observation that a single bout of exercise, which activates AMP kinase, promotes translocation of the glucose transporter GLUT4 and glucose uptake independently of insulin 86 , completely reversed these abnormalities 76,87 . Insulin-resistant individuals also exhibit reduced muscle mitochondrial density, gene expression and function, which impedes lipid oxidation. This, combined with augmented hepatic TAG release, contributes to muscle lipid accumulation. Collectively, these findings suggest a specific phenotype, whereby genetic and/or acquired reductions in muscle mitochondrial function predispose these individuals to sn-1,2-DAG accumulation, activation of PKCθ and PKCε and insulin resistance in muscle, which can be enhanced further by excessive production of reactive oxygen species 88 (Fig. 2b). Such selective muscle insulin resistance also increases cardiometabolic risk owing to increased TAG and VLDL production and subsequent dyslipidaemia. The association between muscle insulin resistance and abnormal mitochondrial function represents a frequently observed feature of the elderly and people prone to or with overt T2D 79,89 .
There is increasing evidence supporting a hypothesis whereby gene variants in mitochondrial DNA (mtDNA) and mitochondrial-function-related nuclear DNA contribute to insulin resistance and T2D 90 or abnormal exercise-induced responses 91 . Gene variants in mitochondrial-function-related nuclear DNA lead to relatively mildly impaired mitochondrial function, whereas classical mtDNA gene variants typically cause a severe reduction in mitochondrial function with neurological deficits and β-cell failure. In contrast to genetic and acquired alterations that lead to mild impairments in mitochondrial activity and a predisposition to ectopic lipid accumulation and insulin resistance, alterations that lead to severe reductions in mitochondrial activity (for example, mtDNA variants) result in increased dependency on anaerobic glycolysis, hyperlactaemia and increased glucose metabolism 92,93,94 . In support of this hypothesis, a recent European GWAS reported that a nonsynonymous variant of N-acetyltransferase 2 (NAT2) is associated with insulin resistance and related traits as well as with decreased adipocyte differentiation, insulin-mediated glucose uptake and increased WAT lipolysis 95 . Silencing or knocking down the mouse NAT2 orthologue, NAT1, induces insulin resistance, glucose intolerance and exercise intolerance 96,97 and is associated with ectopic accumulation of TAG and DAG accumulation and activation of hepatic PKCε and muscle PKCθ 97 . Nat1 −/− mice also display mild reductions in mitochondrial function and altered morphology, demonstrating another genetic link between reduced mitochondrial function, TAG and DAG deposition and nPKC-induced liver and muscle insulin resistance 97 . Further supporting a relevant role of mitochondria for the development of insulin resistance, mice with muscle-specific knockout of sarcolipin, which is required for mitochondrial sarcoendoplasmic reticulum Ca 2+ -ATPase (SERCA) uncoupling and lipid oxidation, develop obesity and DAG–nPKC-mediated muscle insulin resistance, whereas sarcolipin overexpression prevents obesity-induced insulin resistance 98 . Other gene variants may also predispose humans to muscle insulin resistance and T2D independently from altered mitochondrial function, such as the AKT2 partial loss-of-function mutation that results in lower insulin-stimulated muscle and adipose glucose uptake 99 , whereas an activating mutation causes fasting hypoglycaemia 100 . AS160 (also known as TBC1D4) gene variants suggest links between insulin signalling and glucose transport leading to muscle insulin resistance, postprandial hyperinsulinaemia and hyperglycaemia 101,102 . Furthermore, RAC1-mediated glucose transport can become dysregulated in insulin-resistant murine and human skeletal muscle 103 (Fig. 2a,b). These genotypes may have been advantageous for preserving glucose for other tissues in the prehistoric arctic environment.
Causes of diabetes fatigue
First, diabetes can directly cause fatigue with high or low blood sugar levels.
Causes related to blood sugar
• High blood glucose makes your blood “sludgy,” slowing circulation so cells can’t get the oxygen and nutrients they need. Margaret commented, “I can tell if my sugars are high in the morning, because ‘groggy’ doesn’t begin to describe it. ‘Drugged’ is how it feels.”
• Low sugars levels also cause diabetes fatigue, because when blood sugar is low, there is not enough fuel for the cells to work well.
• In addition, high blood glucose can cause diabetes fatigue through inflammation. Blood vessels get inflamed by the sugar. When this happens, according to research, immune cells called monocytes come into the brain, causing fatigue.
Other medical conditions that can cause fatigue
But your diabetes fatigue may not be caused by diabetes at all. Other medical conditions that can cause fatigue include:
• Anemia, or low red blood cell counts. It’s easy to be tested for anemia. If you’ve got it, it’s usually due to deficiency of iron, folic acid, or vitamin B-12, or to heavy menstrual bleeding in women (which results in iron deficiency).
• Low thyroid (“hypothyroidism”) — people with diabetes are more likely than others to have thyroid problems. If your thyroid level is low, you are likely to feel tired, sleepy, and depressed.
• Low testosterone levels, especially in men. Men with diabetes are much more likely to have low testosterone.
• Infections: People with diabetes often have infections they don’t know about. Infections take energy to fight, which can cause fatigue and raise blood sugar levels. A common source is urinary tract or “bladder” infections. They often hurt, but sometimes have no symptoms, except for the fatigue. Silent dental infections and vaginal infections are also common and fatiguing.
• Undiagnosed heart disease: If you get tired after tasks that you used to sail through, it could be time to for a heart check-up.
• Conditions like chronic fatigue and fibromyalgia. These are much more common in women, but men get them too. Fatigue is the main symptom. Many other diseases cause fatigue — you can see the government’s list here.
• Medication side effects: Many drugs for diabetes, blood pressure, depression, pain, and other issues can cause fatigue. Read labels, ask your doctor or pharmacist.
Additional causes of fatigue
Then there are causes that aren’t entirely medical:
• Lack of sleep or poor sleep — Some people are too wound up or too busy to sleep. Or they’re up to use the bathroom all night, or they have obstructive sleep apnea (OSA), which can wake them up many times an hour. If that is happening to you, you are likely to be fatigued during the day.
• Shift work — rotating shifts or working nights — can cause fatigue directly by messing with your body clock or indirectly by disrupting sleep.
• Depression is very common with diabetes. Most depressed people feel fatigued, even if they don’t feel sad. Even at low levels, depression can sap your motivation. Why get up? You can take a free test to see if you are depressed here.
• Doing too much: If you’re ripping and running all day, not taking breaks or even stopping to breathe much, you are courting fatigue. Patti wrote, “I think that forcing myself to do everything is just causing the fatigue to worsen.” She’s probably right.
• Stress: In small doses, psychological or physical stress can give you energy, but if it goes on too long, it will wear you out.
• Diet: Too much carbohydrate — especially refined carbs — can make anyone tired, especially with diabetes. Kat wrote, “now that I am eating a higher protein/fat, lower-carbohydrate diet, I have shaken off that really sleepy/extreme fatigue that I used to have every day.”
• According to WebMD, too much caffeine can cause diabetes fatigue through a rebound effect. They also say that dehydration, or not drinking enough liquid, is a major cause of fatigue.
• Being out of shape or having weak muscles: Not moving our bodies contributes to fatigue. Of course, it’s hard to exercise when you’re fatigued.
• Aging: It is normal to have less energy as we age, but this slowing down should not be dramatic. If loss of energy is rapid or severe, there is something else going on.
This list is getting ridiculously long, and it’s not complete. If you’re dealing with fatigue, perhaps start by evaluating yourself for these possibilities. Then read my piece “Stress and Fatigue” for solutions professionals and our readers have found.
Want to learn how to reduce diabetes fatigue? Read “Recovering From Diabetes Fatigue” and “Diabetes Fatigue — Get Your Energy Back,” by nurse David Spero.
Disclaimer of Medical Advice: You understand that the blog posts and comments to such blog posts (whether posted by us, our agents or bloggers, or by users) do not constitute medical advice or recommendation of any kind, and you should not rely on any information contained in such posts or comments to replace consultations with your qualified health care professionals to meet your individual needs. The opinions and other information contained in the blog posts and comments do not reflect the opinions or positions of the Site Proprietor.
Biological Weathering and Its Deadly Effect on Black Mothers
Imagine for a moment that you’re a very silly 22-year-old driving through Florida sometime around 2009. You’re speeding down a road called Alligator Alley at approximately 92 miles an hour, which is about 20 miles above the speed limit. It’s late. Maybe the windows are down. Maybe the music is blaring. Maybe you’re singing off-key. You’re basically living your best life until police lights appear behind you, and you remember you’re not in a coming-of-age film. You’re a black woman driving alone in the middle of the night. In the South.
This is how I die, you think, as a stoic police officer takes your license and registration from your shaking hand. The police killing of Michael Brown that thrust Black Lives Matter into the national spotlight hadn’t happened yet. But you grew up hearing about Sean Bell and Amadou Diallo, Brown’s forefathers on the list of black people killed by police, his companions in this traumatic, helpless club. You know how dangerous this can be.
The police officer walks away. After what feels like an eternity, he returns.
“For the love of God,” he hisses, handing you back your information. “You really need to slow down.”
You didn’t get a ticket. You really deserved a ticket.
The officer leaves, but your heart won’t stop racing, and your muscles don’t relax. You’re still shaking, and your breathing doesn’t slow. There’s nothing to do but sit there, wading through fear and the feeling that you got lucky, then keep driving.
I was that 22-year-old who thought she was going to die in the middle of the night on a Florida road. I know very well the visceral fear that comes from premature death being an acceptable hazard of the black American experience. I understand what it means for racism to be such a fact of everyday life that my first thought when I got pulled over wasn’t “I hope I don’t get a ticket” but “I hope I make it through this alive.”
The term “weathering” describes how the constant stress of racism may lead to premature biological aging and poor health outcomes for black people, like disproportionately high death rates from chronic conditions such as heart disease, stroke, diabetes, and most cancers.
Mental anguish and stress from “fighting against larger structures and systems can have an impact on your health,” Joia Crear-Perry, M.D., founder and president of the National Birth Equity Collaborative, tells SELF. This, in a nutshell, is weathering.
Weathering plays a significant and intriguing role in conversations about black maternal mortality, a public health crisis based around the fact that black women are three to four times more likely to die from pregnancy-related complications than white women in the United States, according to the Centers for Disease Control and Prevention (CDC). As part of our ongoing series on black maternal mortality, we’re unpacking how weathering works, why it matters even if you’re not pregnant, and what you can do with this information.
Any kind of long-term stress can affect your body. “We’ve learned a lot about what stress does to your body and your organs and how it accelerates the aging of your cells,” Arline Geronimus, doctor of science, professor at the University of Michigan School of Public Health and member of the National Academy of Medicine, tells SELF. “This has helped me understand how lived experiences become biology,” says Geronimus, who first coined the term “weathering” with her landmark 1992 Ethnicity & Disease hypothesis on the subject.
Stress is your body’s natural response to perceived danger. It’s actually meant to be helpful. When you experience stress, your brain’s hypothalamus prompts your adrenal glands to release hormones including adrenaline and cortisol, according to the Mayo Clinic. These hormones can impact a host of bodily functions, like increasing your blood pressure and quickening your heart rate. All of these physiological changes allow you to fight your potential stressor or flee from harm (hence the term “fight-or-flight response”).
To illustrate how this works, Dr. Crear-Perry uses an example far too many black people can relate to: a store employee following you for no reason besides the color of your skin. “Your heart starts racing, and you start breathing faster,” Dr. Crear-Perry says. “That's a natural physiological response to the stress of being a black person in America.”
Stress responses that happen infrequently and last for a few minutes or so are perfectly normal, but chronic stress can be really detrimental to your health. (“Tell me something I don’t know,” you say.) Chronic stress can make you more prone to mental illnesses like depression, according to the American Psychological Association (APA). It can lead to migraines, tension headaches, and backaches. Chronic stress can also impact your blood vessels, arteries, and heart, which over time can raise your cholesterol levels and even increase the risk of a heart attack. Then there’s how you deal with this stress. If it’s by drinking more than a moderate level of alcohol, smoking cigarettes, or other unhealthy behaviors, that can only compound your risk of health issues.
Chronic stress is unhealthy for the average person, but these symptoms can be even more worrisome for pregnant people. If symptoms of stress like trouble falling asleep, loss of appetite, and headaches get severe enough during your pregnancy, they can impact you and your growing fetus, according to the National Institute of Child Health and Human Development (NICHD). High blood pressure—which chronic stress can absolutely help induce—can directly increase the chances of having preterm labor as well as a baby with low birth weight, the NICHD explains. Those kinds of poor birth outcomes were the impetus for Geronimus’s weathering research.
Geronimus came up with the idea of weathering while examining why teen moms have overall higher rates of preterm birth, low birth weight, and infant death, with young black mothers having even higher rates than young white moms. She became interested in this area of study after working with several groups of black teen mothers as a young research assistant. Geronimus’s theory was that if she could take into account the different life experiences between black and white teens (like income levels), birth outcomes would improve the longer people waited to get pregnant, no matter their race. To find her answer, she dug into large pools of data like the CDC’s information on birth outcomes in 1983 among people aged 15 to 34 of various races.
“When I actually studied it, I began to see I was wrong,” Geronimus says.
What Geronimus found was that birth outcomes worsened among black moms as they aged. “If you were black and a teen mom, you had better birth outcomes even when compared to your 20s, and certainly by the mid or late 20s,” Geronimus says. The same wasn’t true for the white moms she studied.
In response to this finding, Geronimus developed the theory that weathering was a form of premature aging due to exposure to social inequity, she explains. The term is meant to capture the positive connotation of weathering (making it through a difficult experience) along with the negative implication (being damaged in the process).
Oppressed groups are essentially put between a rock and a hard place, Geronimus says. “They [are] expected to do things even though they were set up for failure, and if they [succeed] at them, it [exacts] a physical price.”
Since first publishing her theory on weathering, Geronimus has conducted more research to see how it holds up. In 1996 she published a study in Social Science & Medicine that looked at 54,888 births in black and white Michigan residents between the ages of 15 and 34, finding that as the black moms aged, they were more likely to have low birth weight and very low-birth-weight babies. The effect was more severe for black women living in low-income areas, but it persisted no matter their income level.
One prime question in weathering research is how discrimination can lead to tangible negative health outcomes. In 2010, Geronimus and her fellow researchers published a study in Human Nature, examining how telomere lengths differed in 110 black and 105 white women from 49 to 55 years old. Telomeres are “stabilizing caps” located on the ends of chromosomes that protect DNA, sort of like the plastic ends on your shoelaces, Geronimus explains. They naturally shorten during cell division and throughout your aging process, but there’s also research to suggest that environmental factors can speed up that deterioration. A 2013 literature review published in the Journal of Internal Medicine notes that one of the most robust studies on telomere lengths suggested a 25% risk of early death among people with the shortest telomeres. Because of that, Geronimus and her team theorized that telomere lengths could be an indicator of weathering. They found that, based on telomere length, black women in the age range of 49 to 55 were on average 7.5 years “older” biologically than white women of the same age, though they note the various limitations to the study, like small sample size, and say more research is necessary before reaching a definitive conclusion here.
But the ability to measure how overexposure to stress hormones can cause biological damage, known as the allostatic load, may give Geronimus’s theory more scientific credence. Allostatic load is measured through a composite index of lab test results indicating stress-related wear and tear across the body, Geronimus explains. Various research points to racial disparities that can’t be fully attributed to things like differences in income level.
To further illustrate the idea that weathering is a biological process that can happen across socioeconomic status, in 2015 Geronimus published another study on telomere length, this one in the Journal of Health and Social Behavior. The study authors examined the telomere lengths of 239 black, white, and Mexican adults living in Detroit who spanned a range of low to moderate incomes. The researchers found that white residents who lived in poverty had shorter telomere lengths than their white moderate-income counterparts, black residents had equivalent telomere lengths regardless of income level, and Mexican residents living in poverty had longer telomere lengths than their Mexican moderate-income counterparts.
“This [outcome] is actually what my colleagues and I had predicted because [weathering] is not about poverty itself,” Geronimus says. Instead, it’s about how others in your environment treat you based on race, which financial security can’t always change. For instance, middle-income black residents who still had relatively short telomeres were spending time in environments where they were subjected to othering and social isolation, which “was affecting their telomere lengths from a kind of prolonged [physiological] stress,” she explains. This study was also limited by issues like small sample size, but it still adds to the collection of evidence that racism may affect health.
Geronimus’s research on Mexican residents in Detroit (many were born abroad) complements recent research on birth outcomes in African immigrants and U.S.-born black women. A 2017 Medicine study looking at 1,121 black women born in the United States and Africa found that participants who had recently immigrated had lower rates of preterm birth than the U.S.-born black Americans (though they’re certainly not immune from pregnancy and childbirth complications).
“There’s a toll of having to prove yourself all the time and interact with the people who disparage you and oppress you,” Geronimus says.
There isn’t yet a quantifiable amount of stress we can point to that indicates if someone will experience weathering, Geronimus says, or an exact age when its effects begin. But this wealth of research does help challenge the frustrating notion that oppressed people can simply “pull themselves up by their bootstraps” to eliminate disadvantages and disparities.
The concept of weathering explains, at least in part, why factors like education, income, access to health care, and pure willpower can’t fully insulate you from poor health outcomes. However, it’s key to see weathering as one of many frameworks seeking to understand how racialized stress impacts black people, Angela Aina, M.P.H., codirector and research lead of Black Mamas Matter Alliance, tells SELF. As an example, Aina cites the Sojourner Syndrome framework developed by anthropologist Leith Mullings, Ph.D. The Sojourner Syndrome framework is the idea that factors like race, class, and gender all work together to create very real barriers to good health. While a lot of weathering research aims to look at race on its own, the Sojourner Syndrome framework argues that none of these factors can be separated from the others. It was built on the research of Sherman A. James, Ph.D., who invented the term John Henryism, another framework that explores how black people pour a lot of effort into coping with stressors like discrimination, and how that effort can be damaging to their health.
A 2016 study published in Souls: A Critical Journal of Black Politics, Culture, and Society analyzed the way that “respectability behaviors” impact health. As strategies people employ to try to manage other people’s perceptions of them and avoid discrimination, respectability behaviors are an example of the coping efforts described in John Henryism. The study, which included survey data from 3,015 black people over the age of 18 living in Chicago, found that black people who engaged in “vigilance,” or the anticipation of discrimination or racism, had higher reports of chronic illnesses including hypertension and depressive symptoms. This study and its adjoining “vigilance” framework join a long and robust history of research on how navigating everyday life as a black person in America can quite literally be bad for your health.
This brings us to the crux of our exploration: weathering and black maternal mortality. In New York City, a college-educated black woman is three times more likely to experience severe maternal complications than a white woman without a high school education, according to a 2016 "New York City Department of Health and Mental Hygiene’s Severe Maternal Morbidity" report.
Weathering seems to be an inextricable part of black maternal mortality. Pregnancy offers a compelling opportunity to study weathering in a concrete way. It’s a relatively short-term medical condition with very measurable outcomes like birth weight or infant mortality, “whereas things like hypertension or diabetes take decades [to develop], and it’s harder to pinpoint the root cause,” she says.
That also means there tends to be more direct weathering research on infant outcomes, not other reproductive outcomes like maternal mortality. It’s not as though any researcher has been able to study exactly how much of a role weathering plays in the deaths of the black people we lose every year due to pregnancy or childbirth complications. But it’s only logical for a phenomenon that could so impact infant outcomes to have the awful power of harming their pregnant and postpartum parents too. A 2019 study in The Journal of Maternal-Fetal & Neonatal Medicine found that every 1 out of 270 births in California involved both preterm labor and severe maternal health complications. The two are often terribly and closely connected.
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