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Scientists are also learning that visceral fat pumps out immune system chemicals called cytokines — for example, tumor necrosis factor and interleukin-6 — that can increase the risk of cardiovascular disease.
These and other biochemicals are thought to have deleterious effects on cells' sensitivity to insulin, blood pressure, and blood clotting. One reason excess visceral fat is so harmful could be its location near the portal vein, which carries blood from the intestinal area to the liver. Substances released by visceral fat, including free fatty acids, enter the portal vein and travel to the liver, where they can influence the production of blood lipids.
Visceral fat is directly linked with higher total cholesterol and LDL bad cholesterol, lower HDL good cholesterol, and insulin resistance. Insulin resistance means that your body's muscle and liver cells don't respond adequately to normal levels of insulin, the pancreatic hormone that carries glucose into the body's cells.
Glucose levels in the blood rise, heightening the risk for diabetes. Now for the good news. So what can we do about tubby tummies? A lot, it turns out. The starting point for bringing weight under control, in general, and combating abdominal fat, in particular, is regular moderate-intensity physical activity — at least 30 minutes per day and perhaps up to 60 minutes per day to control weight and lose belly fat.
Strength training exercising with weights may also help fight abdominal fat. Spot exercising, such as doing sit-ups, can tighten abdominal muscles, but it won't get at visceral fat.
Diet is also important. Pay attention to portion size, and emphasize complex carbohydrates fruits, vegetables, and whole grains and lean protein over simple carbohydrates such as white bread, refined-grain pasta, and sugary drinks.
Replacing saturated fats and trans fats with polyunsaturated fats can also help. Scientists hope to develop drug treatments that target abdominal fat. For now, experts stress that lifestyle, especially exercise, is the very best way to fight visceral fat. As a service to our readers, Harvard Health Publishing provides access to our library of archived content.
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: Visceral fat accumulation| Pathophysiology of human visceral obesity: an update | We now know that there's far more to the story. Patients with diabetes who used GLP-1 drugs, including tirzepatide, semaglutide, dulaglutide, and exenatide had a decreased chance of being diagnosed…. Exercise and dieting helps you lose belly fat So what can we do about tubby tummies? For women, this can be especially true as body fat tends to shift to the abdomen after menopause. Belly fat also includes visceral fat. CREST, Japan Agency for Medical Research and Development, Tokyo, Japan. |
| Taking Aim at Belly Fat - Harvard Health Publishing - Harvard Health | Studies by Thermogenic stacks et al. The accumulatio way to Viscerla visceral Body composition changes is through losing weight if you are above a Viwceral weight range and Sports stamina elixir a healthy diet. A man with a accumklation that Visceral fat accumulation 40 Antioxidant-rich supplements or more fatt a woman whose waistline measures 35 inches or more is likely to have stores of visceral fat. This important observation suggests that the high intake of dietary fat in men promotes fat accumulation that is rather specific to the abdominal visceral depot. Weinstock, P. Researchers found that having a high WHtR was one of the best indicators that a person with type 1 diabetes also has a high percentage of visceral fat. Estrogen female sex hormone causes fat to be stored in the buttocks, thighs, and hips in women. |
| Adipose tissue - Wikipedia | Visceral fat, on the other hand, lies out of reach, deep within the abdominal cavity, where it pads the spaces between our abdominal organs. Further research is needed to determine whether a significant relationship between alcohol consumption and abdominal obesity exists among women who consume higher amounts of alcohol. G PubMed Abstract CrossRef Full Text Google Scholar. Accepted : 02 October Read more on Diabetes Australia website. A woman whose waist measures 35 inches or more is likely to have excess visceral fat. Journal of Sex Research. |
| Top bar navigation | Based on its location in the body, white fat can be further subcategorized into subcutaneous, visceral, and ectopic fat. The insulin resistance-dyslipidemic syndrome: contribution of visceral obesity and therapeutic implications. Reconstructive surgery is one aspect of treatment. The trouble with belly fat is that it's not limited to the layer of padding just below the skin. Based on our proposed mechanisms, spreading out the amount of dietary fat intake into several smaller meals should reduce the likelihood of abdominal visceral fat accumulation by reducing both the size and number of chylomicrons. Fast facts on visceral fat: Excess visceral fat can cause serious health problems. Stay on top of latest health news from Harvard Medical School. |
| Frontiers | Why Do Men Accumulate Abdominal Visceral Fat? | Explore careers. This, again, is supported by the prolonged elevation of plasma chylomicrons in men Knuth and Horowitz, as well as the higher recovery of the infused lipids in the intestinal mucosa when the intestine is challenged with more fat Lo et al. discovered the protein leptin that the genetically obese mouse lacked. You may opt-out of email communications at any time by clicking on the unsubscribe link in the e-mail. Index of Central Obesity ICO is the ratio of waist circumference and height first proposed by a Parikh et al. About Mayo Clinic. |
Visceral fat accumulation -
Most of the connections are made to the posterior rather than the anterior wall of the abdominal cavity. As such, organs that reside within the posterior wall of the abdominal cavity do not have any mesenteries.
These organs are commonly known as retroperitoneal organs. The two retroperitoneal organs depicted in Figure 1 are pancreas and duodenum. The fat that surrounds these retroperitoneal organs is known as retroperitoneal fat. Note that other retroperitoneal organs, such as kidneys, ascending colon, and descending colon, are not shown in Figure 1.
Figure 1. The storage of dietary triglycerides by abdominal visceral fat. Dietary triglycerides are digested and taken up by the enterocytes that line the intestinal lumen. The enterocytes secrete the dietary triglycerides in the form of VLDLs and chylomicrons to the lamina propria.
Due to their smaller size, some of the VLDLs can readily enter the lumen of the blood capillaries. In contrast, chylomicrons that are produced more by males are more likely to be retained in the lamina propria as they attempt to gain access to the lumen of the lymphatics.
The higher retention of chylomicrons in the lamina propria predisposes their triglycerides to LPL hydrolysis. The liberated fatty acids, which are the products of LPL hydrolysis, can then be delivered to the abdominal visceral adipocytes that are located within the retroperitoneum and mesenteries.
The fat that lies within the retroperitoneum is called retroperitoneal fat, and the fat in the mesenteries is known as intraperitoneal fat. The intraperitoneal fat depots shown here are mesocolonic, lesser omental, greater omental, and mesenteric fat.
Note that the liberated fatty acids supply the abdominal visceral adipocytes prior to the subcutaneous adipocytes. In addition to adhering the gastrointestinal organs to their abdominal wall, mesenteries protect numerous nerves, blood vessels, and lymphatic vessels of the gastrointestinal system.
Importantly, mesenteries are also capable of storing a significant amount of fat. The greater omentum, lesser omentum, mesentery proper, and mesocolon are examples of mesenteries.
As indicated in Figure 1 , the fat that is located within these mesenteries is known as the greater omental fat, lesser omental fat, mesenteric fat, and mesocolonic fat, respectively. The fat in these mesenteries is collectively referred to as intraperitoneal fat.
Both intraperitoneal fat and retroperitoneal fat constitute abdominal visceral fat, which explains why many investigators include retroperitoneal fat when measuring abdominal visceral fat Hung et al.
There are several reasons to consider the retroperitoneal fat as part of the abdominal visceral fat. First, retroperitoneal fat surrounds retroperitoneal organs. Thus, it should be categorized as visceral instead of ectopic or subcutaneous fat.
Second, the lymph fluid of the gastrointestinal tract drains through the smaller lymphatic vessels within the mesenteries before entering the larger lymphatics.
The larger lymphatics, such as cisterna chyli, are retroperitoneal. Consequently, the adipocytes that are present in the mesenteries and retroperitoneum receive the same supply of lipid-rich chyle. This chyle will eventually be drained into the systemic blood circulation before supplying the subcutaneous fat.
Hence, from the nutrient supply perspective, retroperitoneal fat is more similar to intraperitoneal fat than subcutaneous fat. For further discussions on the anatomy of the gastrointestinal circulation, please refer to our previously published paper Nauli and Nauli, Third, unlike subcutaneous fat, both retroperitoneal and intraperitoneal fat increase the risk of metabolic syndrome Hung et al.
Therefore, it is conceivable that abdominal visceral fat should include both intraperitoneal and retroperitoneal fat. Figure 2 shows how different types of body fat relate to abdominal visceral fat. Figure 2. Types of body fat in relation to abdominal visceral fat.
Body fat can be categorized into brown, beige, and white fat. Based on its location, white fat can be further categorized into ectopic, subcutaneous, and visceral fat.
Some of the examples of ectopic fat are intrahepatocellular, intrapancreatic, intramyocellular, and intracardiomyocellular fat. Subcutaneous fat includes abdominal, femoral, and gluteal subcutaneous fat.
Visceral fat includes epicardial, retroperitoneal, and intraperitoneal fat. The intraperitoneal fat can be further subcategorized into mesocolonic, lesser omental, greater omental, and mesenteric fat. Due to their tendency of accumulating abdominal visceral fat Grauer et al.
The excessive accumulation of abdominal visceral fat is also known as android obesity. In contrast, the pear-shaped is often ascribed to pre-menopausal women because of their tendency of accumulating subcutaneous fat in the thigh femoral and buttock gluteal regions Karastergiou et al.
The obesity resulted from the predominant subcutaneous fat accumulation is also known as gynoid obesity. A common misconception is that beer consumption can specifically lead to belly fat accumulation.
Therefore, it is unlikely that beer consumption specifically increases the abdominal visceral fat or is particularly responsible for android obesity. Although the abdominal subcutaneous fat and the intrahepatocellular fat are associated with a higher risk of mortality in men, only the abdominal visceral fat is a strong independent predictor of mortality in men Kuk et al.
The association of abdominal visceral fat with mortality is not unique to men as abdominal visceral fat is also a strong predictor of mortality in obese women Koster et al. Consequently, it is important to understand the pathogenesis of abdominal visceral fat and its association with metabolic complications.
Obesity can impede the functions of microvasculature. Studies in male hamsters have revealed that android obesity is associated not only with insulin resistance but also a diminution of capillary density and an increase in macromolecular permeability Costa et al. This microvascular dysfunction may eventually lead to the development of hypertension Covassin et al.
Interestingly, the male hamsters that were subjected to the high-fat diet in these studies accumulated fat almost exclusively in the abdominal visceral region with minimal fat accumulation in the subcutaneous region.
This important observation suggests that the high intake of dietary fat in men promotes fat accumulation that is rather specific to the abdominal visceral depot.
The increase in vascular permeability in the android obesity described above Costa et al. In this regard, the endothelial cells that line the affected vasculatures may be a key contributor in the development of android obesity as suggested in a recent proposed two-way communication hypothesis of vascular dysfunction in obesity Graupera and Claret, We have previously described how android obesity may lead to insulin resistance Nauli, As the abdominal visceral fat accumulates, macrophages infiltration increases Xu et al.
The infiltrating macrophages are known to release inflammatory cytokines. These cytokines, which include TNFα, are capable of causing the surrounding abdominal visceral adipocytes to become insulin resistant and liberate their fatty acids Samuel and Shulman, This flux of fatty acids is detrimental to the liver and pancreas Matsuzawa et al.
Note that the flux of fatty acids to the liver also occurs after a bolus feeding of triglycerides. Bolus feeding of fat has been shown to increase unesterified fatty acid concentration in the portal vein Kristensen et al.
Therefore, it is possible that both the abdominal visceral fat and the frequent consumption of high-fat diet contribute to the pathogenesis of metabolic syndrome through the increased flux of fatty acids to the portal venous circulation. Perhaps it is worthwhile to examine the results of the omentectomy studies.
One of the earliest omentectomy studies shows that patients who received omentectomy and adjustable gastric banding had a better metabolic profile than those with the adjustable gastric banding alone Thorne et al.
The patients with omentectomy and adjustable gastric banding lost more weight than the patients with adjustable gastric banding alone, albeit not significantly. Studies by Dillard et al. On the contrary, studies by Fabbrini et al. Several other studies did not also show any significant metabolic improvements in the omentectomy group Csendes et al.
Based on the discussion above, it can be concluded that more studies are needed to elucidate the exact roles of the abdominal visceral fat in the pathogenesis of metabolic syndrome. It is clear, however, that abdominal visceral fat is associated with many detrimental effects Booth et al.
The underlying mechanisms of why men are more likely than pre-menopausal women to accumulate abdominal visceral fat remain unclear. Evidence indicates that once dietary fat is absorbed by the gut, the intestinal lipoproteins produced between males and females are not identical Vahouny et al.
How these intestinal lipoproteins may contribute to the sex differences in the regional body fat distribution will be discussed below. Accumulation of fat is the result of a higher calorie intake relative to the energy expenditure. From the adipocyte perspective, this corresponds to more uptake of nutrients than the breakdown of fat by adipocytes.
The fat catabolism of adipocytes, also known as lipolysis, is mediated partly by epinephrine. Upon binding of epinephrine to β adrenergic receptors, lipolysis is stimulated.
On the contrary, the binding of epinephrine to α2A adrenergic receptors results in the inhibition of lipolysis Richelsen, In essence, β receptors are lipolytic and α2A receptors are anti-lipolytic. Studies have shown that estrogen reduces the lipolysis in the gluteal subcutaneous adipocytes Gavin et al.
The reduced lipolysis in the gluteal subcutaneous adipocytes in women is likely due to estrogen receptor α-mediated increase in α2A receptors. The estrogen-stimulated increase of these anti-lipolytic receptors in the subcutaneous adipocytes, but not in the abdominal visceral adipocytes, may contribute to the more pronounced lipolysis in the abdominal visceral adipocytes relative to the subcutaneous adipocytes in women Pedersen et al.
The net fat accumulation in a particular fat depot, however, depends not only on its adipocyte lipolysis but also on the nutrient uptake of its adipocytes as well as its total number of adipocytes. Since estrogen is capable of stimulating human pre-adipocyte proliferation Anderson et al.
In fact, studies comparing the lipolysis and nutrient uptake of various fat depots indicate that women have more lipolysis than men in the lower body fat depot, whereas men have more lipolysis than women in the abdominal visceral fat depot Santosa and Jensen, The studies suggest that relative to lipolysis, fat uptake contributes more significantly to sex differences in body fat distribution.
In other words, women accumulate more fat in the subcutaneous depot primarily because that depot takes up more fat in women than men. Likewise, men accumulate more fat in the abdominal visceral depot because their fat depot takes up more fat than women.
Some factors contributing to the tendency of non-obese women to accumulate subcutaneous fat include their high LPL activities in subcutaneous fat depots Arner et al. LPL activities are critical for body fat accumulation Serra et al.
A recent study shows that testosterone is capable of suppressing the LPL activity and fat storage in the femoral region Santosa et al. Another factor that promotes subcutaneous fat accumulation in non-obese women is their high hepatic-derived lipoprotein catabolic rate, which partly explains why they have lower plasma concentrations of apolipoprotein B Watts et al.
In addition to their high catabolic rate, women are also capable of secreting triglyceride-rich VLDLs when their liver is challenged with more fat Hodson et al. Consequently, women are more effective than men in redirecting fat storage from liver to subcutaneous fat Palmisano et al.
It can be concluded that women accumulate more fat in the subcutaneous depot because they have higher subcutaneous fat LPL activities and higher catabolic rate of hepatic-derived lipoproteins. The factors that allow men to accumulate more fat in the abdominal visceral depot will be discussed below.
The fat that is taken up by the adipocytes is primarily from lipoproteins, lipid particles with triglycerides in their core. The fact that men and women have different intestinal lipoproteins can potentially determine which body fat depot the dietary fat will be deposited to.
The organ that arguably secretes the most amount of fat is the small intestine, particularly during the postprandial state. Recall that the small intestine is surrounded by the abdominal visceral fat. Therefore, it is not surprising that the abdominal visceral fat can take up quite a significant amount of dietary fat from the intestinal lipoproteins.
These studies further support the notion that sex difference in regional body fat distribution is primarily determined by fat uptake rather than lipolysis. Dietary fat is digested and absorbed by the small intestine. Unlike VLDLs that can be produced during the preprandial states, the production of chylomicrons is primarily driven by dietary fat intake Nauli et al.
Importantly, when the small intestine is challenged with a higher amount of fat, it will produce bigger chylomicrons Lo et al. These bigger chylomicrons tend to accumulate in the intestinal mucosa, as reflected by the higher recovery of the intraduodenally infused lipids in the intestinal mucosa, lower recovery in the lymph, and minimal recovery in the lumen at the end of the 6-h study.
Since men generally consume a higher amount of dietary fat due to their higher energy intake Wright and Wang, , they are expected to produce bigger and more chylomicrons than women.
Studies comparing the postprandial chylomicrons in the plasma, in fact, indicate that chylomicrons transport significantly more dietary fat in men than in women Knuth and Horowitz, The elevated plasma level of postprandial chylomicrons is also more prolonged in men than in women, suggesting further that it takes more time for men to transport bigger chylomicrons to the general circulation.
Since the male participants were provided with more dietary fat in the studies, it remains to be determined if the reported effects were primarily due to their higher intake of fat.
However, considering that men do normally have a higher dietary fat intake than women Wright and Wang, , these studies are still highly relevant physiologically.
Of note, all of the female participants in the studies were in their follicular phase. Since the serum level of estrogen is significantly higher than progesterone in the mid-to-late follicular phase, the estrogen effect on the size of chylomicrons warrants more investigation. Studies utilizing rodents indicate that even with a comparable amount of fat entering the lumen of the digestive tract, the chylomicrons produced by males transport more dietary fat than those produced by females; and the VLDLs produced by females transport more dietary fat than those produced by male Vahouny et al.
From the animal to human studies discussed above, we can conclude that men transport more dietary fat through chylomicrons most likely because these chylomicrons are bigger and more than those of women.
There are several similarities and differences between chylomicrons and intestinal VLDLs. Regarding their similarities, both are apolipoprotein Bcontaining lipoproteins. They are also secreted to the capillary-rich lamina propria by the enterocytes see Figure 1. However, their transport routes are quite different, which may determine the fat depot they will preferentially supply their dietary fat to.
Chylomicrons preferentially promote the accumulation of the abdominal visceral fat. High-fat meal, which triggers more chylomicron production, decreased the proportions of meal fat stored in the subcutaneous fat of both men and women Votruba and Jensen, The unaccounted for meal fat in that study was likely stored in the abdominal visceral fat.
It is important to note that the unaccounted for meal fat was found previously to be correlated with the amount of abdominal visceral fat Romanski et al. Since the lymphatic capillaries of the intestine allow bigger particles to enter their lumen relative to the blood capillaries, the lymphatic system is the predominant transport route for most of the chylomicrons.
In addition to the transport by the lymphatics, VLDLs are capable of entering the lumen of the blood capillaries Takahara et al.
Particles as large as 30 nm in diameter have been shown to pass through the walls of the abdominal visceral blood capillaries Simionescu et al. Due to the fact that chylomicrons transport more dietary fat in males than in females, it is not surprising that males also have a higher lymphatic transport of dietary triglycerides than females Vahouny et al.
Relative to the blood circulation, the lymphatic circulation is a low-pressure system that depends on the contraction of the surrounding muscles, such as the diaphragm and other abdominal muscles, to propel the lymph fluid. Consequently, the movement of the chylomicrons within the lamina propria and low-pressure lymphatics becomes a challenge during the postprandial state.
This, again, is supported by the prolonged elevation of plasma chylomicrons in men Knuth and Horowitz, as well as the higher recovery of the infused lipids in the intestinal mucosa when the intestine is challenged with more fat Lo et al. Abdominal visceral fat accumulation has also been shown to correlate significantly with the delayed in postprandial lipid metabolism Taira et al.
Electron microscopy studies also show that during the postprandial state the lipoproteins in the lamina propria are bigger than those in the lymphatic lumen, further supporting the notion that chylomicrons do not enter the lymphatic lumen as readily as their smaller counterparts VLDLs Takahara et al.
Importantly, unlike the lumen of the blood capillaries, the lamina propria and the lymphatic lumen are visibly congested with chylomicrons. The retention of chylomicrons in the lamina propria may predispose their triglycerides to the LPL hydrolysis.
Although it has been reported that mesenteric fat expresses LPLs Shimomura et al. As mentioned above, the LPL activities in the subcutaneous fat depots are generally higher in women, particularly in the lower part of the body Arner et al.
LPLs can be tethered in the extracellular matrix by the HSPGs Young et al. Therefore, it is tempting to speculate that relative to VLDLs, chylomicron triglycerides are more likely to be hydrolyzed by LPLs due to their higher retention in the lamina propria.
Within the fat adipose tissue of CCR2 deficient mice , there is an increased number of eosinophils , greater alternative Macrophage activation, and a propensity towards type 2 cytokine expression.
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Loose connective tissue composed mostly by adipocytes. For the fictional creature from Doctor Who, see List of Doctor Who universe creatures and aliens 0—9, A—G § Adipose. See also: Fat. Adipose tissue is one of the main types of connective tissue.
See also: Abdominal obesity. See also: Body fat percentage. Main article: Brown adipose tissue. Main article: Genetics of obesity § Genes.
See also: Bioelectrical impedance analysis. Stem Cells and Development. doi : PMC PMID Endocrine Reviews. The Journal of Clinical Endocrinology and Metabolism. ImmunoTargets and Therapy. Bibcode : Natur. S2CID The American Journal of Clinical Nutrition.
The Fats of Life. Cambridge University Press. ISBN Prostaglandins, Leukotrienes, and Essential Fatty Acids. Deutsches Ärzteblatt International. September Diabetes Care. American Journal of Physiology. Endocrinology and Metabolism. International Journal of Obesity and Related Metabolic Disorders.
European Journal of Nutrition. American Journal of Human Biology. Archived from the original on Retrieved See: Andrews M Yahoo Health. Women's Health. The Brigham Intensive Review of Internal Medicine 2nd ed. New York, NY: Oxford University Press. Retrieved August 3, International Journal of Obesity.
Obesity Reviews. November Medicine and Science in Sports and Exercise. Metabolic Syndrome and Related Disorders. April San Francisco, Calif. Journal of Bone and Mineral Research.
February June August July International Journal of Endocrinology. Journal of Physical Activity and Health. Quarterly Journal of Experimental Physiology and Cognate Medical Sciences. Frontiers in Neuroscience. The American Journal of Cardiology. Archived from the original on December 20, Proceedings of the National Academy of Sciences of the United States of America.
Bibcode : PNAS.. Hormone and Metabolic Research. PLOS ONE. Bibcode : PLoSO Stem Cells Translational Medicine. Acta Physiologica. FASEB Journal. Physiological Reviews. August 31, Frontiers in Physiology.
Trends in Biochemical Sciences. Frontiers in Endocrinology. The New England Journal of Medicine. Nature Medicine. Current Opinion in Endocrinology, Diabetes, and Obesity. The Journal of Biological Chemistry. Nature Cell Biology. Bioscience Reports. Cell Metabolism. January Hormone Molecular Biology and Clinical Investigation.
Subcutaneous fat is located between the skin and the outer abdominal wall. Body fat, or adipose tissue, was once regarded as little more than a storage depot for fat blobs waiting passively to be used for energy.
But research has shown that fat cells — particularly visceral fat cells — are biologically active. One of the most important developments [since the mids] is the realization that the fat cell is an endocrine organ, secreting hormones and other molecules that have far-reaching effects on other tissues.
Before researchers recognized that fat acts as an endocrine gland, they thought that the main risk of visceral fat was influencing the production of cholesterol by releasing free fatty acids into the bloodstream and liver.
We now know that there's far more to the story. Researchers have identified a host of chemicals that link visceral fat to a surprisingly wide variety of diseases.
Subcutaneous fat produces a higher proportion of beneficial molecules, and visceral fat a higher proportion of molecules with potentially deleterious health effects. Visceral fat makes more of the proteins called cytokines, which can trigger low-level inflammation, a risk factor for heart disease and other chronic conditions.
It also produces a precursor to angiotensin, a protein that causes blood vessels to constrict and blood pressure to rise.
A tape measure is your best home option for keeping tabs on visceral fat. Measure your waistline at the level of the navel — not at the narrowest part of the torso — and always measure in the same place.
According to official guidelines, the bottom of the tape measure should be level with the top of the right hip bone, or ilium — see the illustration — at the point where the ilium intersects a line dropped vertically from the center of the armpit.
Don't suck in your gut or pull the tape tight enough to compress the area. In women, a waist circumference of 35 inches or larger is generally considered a sign of excess visceral fat, but that may not apply if your overall body size is large.
Rather than focus on a single reading or absolute cut-off, keep an eye on whether your waist is growing are your pants getting snug at the waist? That should give you a good idea of whether you're gaining unhealthy visceral fat.
Visceral fat can be measured in a variety of ways. CT scans and full-body MRIs are the most precise, but they are expensive and rarely available, so investigators often use estimates based on waist circumference or waist size in proportion to height see "Gut check".
To ensure that they're not just measuring overall obesity, researchers also check whether a person's waist circumference is higher than average for her or his body mass index BMI.
Cardiovascular disease. Several studies have documented this effect. For example, a large study of European women ages 45 to 79 concluded that those with the biggest waists and those with the largest waists in relation to their hip size had more than double the risk of developing heart disease.
The risk was still nearly double even after adjustment for several other risk factors, including blood pressure, cholesterol, smoking, and BMI. Higher visceral-fat volume also has a deleterious impact on several other heart disease risk factors.
It's associated with higher blood pressure, blood sugar levels and triglyceride levels, and lower levels of HDL good cholesterol. Taken together, these changes, known as metabolic syndrome, create a serious risk for cardiovascular disease and type 2 diabetes.
Researchers at Kaiser Permanente found that people in their early 40s with the highest levels of abdominal fat, compared with those who had the least abdominal fat at that age, were nearly three times more likely to develop dementia including Alzheimer's disease by their mids to early 80s.
Dementia was not associated with increased thigh size. The risks were highest for women who were both large-waisted and overweight or obese.
The investigators believe that belly fat raises the risk of asthma more than other poundage because it has inflammatory effects throughout the body, including in the airways. Breast cancer. A combined analysis of several studies found that premenopausal women with abdominal obesity the largest waist size in proportion to their height were at greater risk for breast cancer.
Large waists were also linked to breast cancer risk among postmenopausal women, but that effect was not significant once BMI was taken into account.
Colorectal cancer. People with the most visceral fat have three times the risk of developing colorectal adenomas precancerous polyps than those with the least visceral fat.
The relationship was found after many other risks were accounted for. The researchers also confirmed that adenomatous polyps in the colon are associated with insulin resistance, which may be the mechanism that increases the cancer risk. Where you tend to gain fat depends on your genes, your hormones, your age, your birth weight smaller babies more readily add belly fat later in life , and whether you've had children women who have given birth tend to develop more visceral fat than women who haven't.
As young adults, women on average have less visceral fat than men, but that changes with menopause. You can't change your birth weight or your genes, and you can't hold off menopause.
But there are several ways you can minimize the accumulation of visceral fat. The good news is that because it's more readily metabolized into fatty acids, it responds more efficiently to diet and exercise than fat on the hips and thighs.
Excess intra-abdominal adipose aaccumulation accumulation, often termed visceral accumulatikn, is part of a phenotype including dysfunctional subcutaneous adipose tissue Vissceral and ectopic triglyceride storage Vitamin B for carbohydrate metabolism related to clustering cardiometabolic risk Cornmeal recipes. Sport-specific performance tips increased Gat fatty acid availability; adipose tissue release of Sport-specific performance tips cytokines; liver insulin resistance and Vksceral increased liver Acdumulation synthesis and secretion; cacumulation clearance Viscdral Sports stamina elixir lipoproteins; presence of Gat, dense LDL particles; and reduced Viscreal cholesterol accunulation are among the many metabolic alterations closely related to this condition. Age, gender, genetics, and ethnicity are broad etiological factors contributing to variation in visceral adipose tissue accumulation. Specific mechanisms responsible for proportionally increased visceral fat storage when facing positive energy balance and weight gain may involve sex hormones, local cortisol production in abdominal adipose tissues, endocannabinoids, growth hormone, and dietary fructose. Physiological characteristics of abdominal adipose tissues such as adipocyte size and number, lipolytic responsiveness, lipid storage capacity, and inflammatory cytokine production are significant correlates and even possible determinants of the increased cardiometabolic risk associated with visceral obesity. Thiazolidinediones, estrogen replacement in postmenopausal women, and testosterone replacement in androgen-deficient men have been shown to favorably modulate body fat distribution and cardiometabolic risk to various degrees. However, some of these therapies must now be considered in the context of their serious side effects.
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