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DEXA Scans

Ron Put

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So, I got my first DEXA scan last week.

I did it mostly to check if my Withings Cardio Scale was accurate in its estimate of 11% body fat. The DEXA scan came up with 13.5%, which is relatively close, I guess.

Withings nailed the Bone Mineral Content (BMC) at 6.4 - 6.5 (DEXA scan 6.4) and Lean Mass at 123.5 lbs (DEXA scan 124.1).

Here is a shot of some of the other data:

Where on the body fat/bone density scale are most of those who frequent this forum? I remember seeing scans from AI and Saul, but wondering about the rest.



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Re: visceral fat: "This number should be as low as possible, with a target of zero VAT". 

Well, that is what I thought also - ideally you should have 0% VAT. A few weeks ago, I was talking to a doctor about my 8 day water only fast, and I explained that one reason why I exercised during the fast was that I wanted to burn off as much visceral fat as possible, and my understanding was that visceral fat is the first fat to go when fasting/losing weight (you can lose muscle and bone too). Then the doctor goes (I'm paraphrasing), "well, you don't want to have absolutely zero visceral fat, you need a little, because your organs need a matrix to hold them and it has some hormonal function too. You want very little, but not zero." I was shocked, because I never heard that before and it went against all I read about visceral fat, but what do I know, I'm not a medical scientist, so I didn't contradict her. 

I've never had a DEXA scan, but I am not sure I'm a candidate, as I have some titanium implants in my arms (motorcycle accident), so that might mess with the measurements. 

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9 hours ago, TomBAvoider said:

You want very little, but not zero.

That seems perfectly sensible.   Visceral fat has  important biological functions,  which, arguably,  may even become more important as one grows old.   Clearly VAT should be kept low,  but eliminating it entirely seems pretty dicey, to put it mildly.  But, still,  it's something Fernando Gabriel might want to  research in depth.

Some articles I've read recently on this topic:


Fat fights back (2018)


[...]Visceral fat is an immunological organ that provides fuel for the immune system, generates pro-inflammatory cytokine mobilization, and houses phagocytic cells that mop up bacteria that escape the gut.




Appreciating the defensive function of fat also explains why belly fat can be caused by unhealthy microbial communities in the microbiome, otherwise known as dysbiosis.



In other words, accumulating fat is a predictable response, not just to excess calories, but also to microbial threats. It’s immune function is a two-edged sword that can protect us, and also leads to smoldering inflammation that has harmful long term effects on health and longevity.


Get to know the omentum: The apron of fat that protects your abdomen (2017)


[...]The omentum's immune functions come from groups of small, white filters located among the fat cells. Anatomists first discovered these cell clusters in rabbits around 1874, giving them the name milky spots. Recent research has shown that they aid the omentum by collecting information about the health of the abdominal cavity. While the size and shape of the omentum varies, milky spots speckle the entire tissue and serve as a filter for surrounding fluid.

"The fluid around the abdominal organs doesn't just sit there, it circulates through the milky spots," says Troy D. Randall, a clinical immunologist at the University of Alabama at Birmingham, who co-wrote the review with postdoctoral fellow Selene Meza-Perez. "Milky spots collect cells, antigens, and bacteria before deciding what's going to happen immunologically."

The milky spots' analyses cause the omentum to respond immunologically by releasing inflammatory molecules, tolerating the presence of an antigen, or beginning the process of fibrosis. Humans develop milky spots in their omentum during early development, before bacteria even appears, indicating its role as a primary immune organ.

Unfortunately, even protective organs make mistakes. "In concerns to tumor cells, the omentum makes the wrong decision," Randall says. "It decides to provide tolerance instead of immunity." While tumors of the omentum are uncommon, the circulating fluids bring back cancer cells into the milky spots, where they get trapped like grass in a pool filter, promoting metastasis. It is a breeding ground for aggressive tumors such as in ovarian and gastrointestinal cancer.

Scientists hope to target these sites of tumor growth with therapies that can control abdominal tumors and assist anti-tumor immunity. "If we can figure this out, then we can start really making inroads on cancer treatments because, in most cases, you don't even catch ovarian cancer until it metastasizes," Randall says. "Understanding how cancer changes the immune system will lead us directly to ways to intervene and, hopefully, start to turn things around."


Nutrition, the visceral immune system, and the evolutionary origins of pathogenic obesity (2019)


[...]Fat tissue is sometimes called an “endocrine organ” because its products affect systemic metabolism and immune responses (7, 8). But this does not distinguish between subcutaneous and visceral fat tissue. VAT has been seen as a storage- and command-center that influences energy redistribution during nutritional emergencies, arguably to protect the brain (9).

Without denying the importance of this and other possible functions, the visceral fat depots can also be seen as intraabdominal adipo-immune organs (10). VAT adipocytes (fat cells), like those of lymph nodes (11), are specialized to sequester the particular diet-derived polyunsaturated fatty acids required for immune activities (12), helping to free VAT immune cells from the vagaries of dietary availability that could compromise a rapid and energetically costly immune response (8).

They are also specialized to respond to immune-related signals (e.g., inflammation-associated TNF-α, IL-6, IL-4) and when activated they facultatively increase numbers of receptors for these and perhaps other cytokines (12).

The omentum has been called “the abdominal policeman” [see ref. 13, after Morison (14)] for its multiple lines of defense against intraperitoneal pathogens and foreign matter (SI Appendix, Appendix 3 discusses types of infection subject to omental defenses).

In a nonobese individual, the greater omentum is a loosely hanging fold of the peritoneum that is moved within the peritoneal cavity by respiratory movements, intestinal peristalsis, and general body activity (13, 15). It adheres (through the rapid production of fibrin) to foreign bodies, wounds, and other sites of inflammation and infection, acting like a bandage laden with antibiotic and healing agents. Phagocytes (macrophages and others) ingest bacteria and particulate foreign matter and transport them to the omentum.

The omentum itself encapsulates larger foci of infection and seals microperforations with collagen, thus limiting the spread of infection while stimulating revascularization and tissue regeneration (reviewed in ref. 13).

Within the omentum immune activities are centered in lymph node-like “milky spots.” When activated by the presence of bacteria, the bacterial endotoxin lipopolysaccharide (LPS), or the inflammation-associated cytokine TNF-α, neutrophils (white blood cells of the innate immune system) rapidly move from the blood to milky spots, where they kill accumulated bacteria (16, 17). Unlike lymph nodes, milky spots are unencapsulated, and they enlarge and become more numerous during pathogen-induced endotoxemia, sepsis, and chronic inflammation (18).

The remarkable immune and healing powers of the omentum are dramatized by the surgical practice, more than 100-years-old and still used, of placing surgically devised omental flaps on sites within the abdomen, and even (via a small incision in the diaphragm) on the heart when recovery is threatened by severe postoperative infection (13, 15, 19). A possible role in the dissemination phase of abdominal cancer metastasis, especially of ovarian cancer, is proposed in SI Appendix, Appendix 4.

Mesenteric VAT, which surrounds the small intestine, is “the first line of defense” against pathogens and endotoxins translocated from the intestine to the circulation (11). Mesenteric immune activities occur in small fat-associated lymphoid clusters (FALCs), which resemble milky spots in being unencapsulated, in becoming more numerous in response to inflammation (20), and in having extensive lymphatic, arterial, and venous capillaries. Unlike the milky spots, FALCs are not open to the peritoneal cavity. Instead, they process pathogens and bacterial endotoxins that have entered the blood after crossing the semipermeable mucous and endothelial barrier between the lumen of the small intestine and the blood vessels.

Endopathogenic diarrheal bacteria, such as wild-type Escherichia coli, can damage the intestinal barrier (21); and intestinal parasites sometimes pass, along with LPS, into the blood exposed to mesenteric FALCs (2224). Hyperpermeability of the gut barrier (“leaky gut”), which can occur with high-fat and high-fructose diets and in extreme childhood malnutrition (see below), can lead to pathogen-induced endotoxemia, (typified by presence of LPS in the blood), which activates immune responses of the mesenteric FALCs (25), as well as stimulating an inflammatory response in the omentum (26).

The portal-vein connection to the liver of these two VAT structures is an anatomical indicator of their immune importance. The blood from both mesenteric and omental VAT, joined by other abdominal tributaries, is met at the entry point to the liver by an array of immunologically important cells: specialized fat cells (stellate cells) and macrophages (Kupffer cells) that parallel and complement the immune functions of those found in VAT (SI Appendix, Appendix 5). Only after processing by this double filter of immune defenses in liver and VAT does the viscerally exposed blood enter the general circulation.


The Contribution of Age-Related Changes in Adiposity to Inflammation and Disease

(see charts with flattened J-shaped curves for visceral fat and mortality risks, and interesting  group photos of rowers young and old.)

Counterintuitive relationship between visceral fat and all-cause mortality in an elderly Asian population (2014)


Edited by Sibiriak
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Good point, Tom, and good citations, Sibiriak.

The studies below may add further clarification about the role of visceral fat:

Fat Distribution and Mortality: The AGES-Reykjavik Study


In men, every standard deviation (SD) increment in thigh intermuscular fat was related to a significantly greater mortality risk (HR:1.17, 95%CI:1.08–1.26) after adjustment for age, education, smoking, physical activity, alcohol, BMI, type 2 diabetes and coronary heart disease. In women, visceral fat (per SD increment) significantly increased mortality risk (HR:1.13, 95%CI:1.03–1.25) while abdominal subcutaneous fat (per SD increment) was associated with a lower mortality risk (HR:0.70; 95%CI:0.61–0.80). Significant interactions with BMI were found in women indicating that visceral fat was a strong predictor of mortality in obese women while abdominal and thigh subcutaneous fat were associated with a lower mortality risk in normal and overweight women.


Fat distribution is associated with mortality over 11 years of follow-up independent of overall fatness. The divergent mortality risks for visceral fat and subcutaneous fat in women suggest complex relationships between overall fatness and mortality."

Visceral Fat Is an Independent Predictor of All‐cause Mortality in Men

"Visceral fat is a significant predictor of mortality in men after adjustment for age, follow‐up time, subcutaneous fat, and liver fat. These findings underscore the importance of setting abdominal obesity as a primary target for obesity reduction and, consequently, the need to educate health care practitioners on the importance of routine measurement of visceral fat. Although we measured visceral fat directly by CT scans in this study, waist circumference provides a reasonable approximation of visceral fat in clinical settings."


Abdominal obesity and mortality: The Pennington Center Longitudinal Study

"The results of this study demonstrate an independent effect of VAT on all-cause mortality rates in a sample of white men and women. The magnitude of the association after adjustment for SAT (HR=1.72; 1.20–2.47) is similar to that obtained by Kuk et al.7 (RR=1.93; 1.15–3.23) in men, and McNeely et al.8 (HR=1.47 (1.14–1.89) in Japanese Americans. All three studies have demonstrated that the association between VAT and mortality is independent of several covariates. Among Japanese Americans, the association between VAT and mortality was reduced somewhat after adjustment for body mass index (RR=1.34 (0.99–1.82); however, in this study, the inclusion of body mass index as an additional covariate in Model 2 did not reduce the strength of the association (HR=1.66; 1.07–2.57). These human studies are supported by research that shows that the surgical removal of VAT in rats results in higher mean and maximum lifespan, compared with ad libitum fed rats.12

These results support the use of VAT as a primary target for obesity-reduction strategies. Lifestyle-based interventions such as diet and physical activity have been shown to significantly reduce VAT even in the absence of weight loss.13 VAT is currently not routinely measured in clinical practice, in part due to the requirement of magnetic resonance imaging or CT. However, recent technological advances may allow for the quantification of VAT using other modalities such as dual-energy X-ray absorptiometry."

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Thank you, Sibirak and Ron. This is fascinating - a lot of this is new to me, so I appreciate the education. As usual, things are a lot more complicated in biology, and this VAT thing is no different. Awareness that things are complicated, has led me already years ago, to hold my convictions "lightly". I know this and that, but I don't KNOW. I'm always ready to revise my views when new info comes out, and so, it seems sensible never to get too attached to any conclusion. Speaking of "conclusion", at uni, my degree was philosophy, and there's an old philosophy joke that goes "'conclusion' is the name of the place you stop at when you are tired of thinking". 

What the heck is this then, when you see texts like this, which Ron showed in the shot: This number should be as low as possible, with a target of zero VAT.

I guess it's plain wrong then? Can't trust anything I suppose. Now I'm worried that as a result of my "8 day water-only plus exercise fast" stunt, I've burned off too much VAT - certainly my belly is flat (if not slightly concave - wrapped around muscles 'six-pack').

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Hi Tom!

Zero VAT is as unobtainable as zero subcutaneous fat.  The only way to get either of these numbers to zero is to be dead.

Since you are not dead, your VAT is not -- and never will be, while you're alive -- zero.  The (presumably) small amount of VAT that you have evidently does perform some essential tasks -- but you don't need more VAT to accomplish these tasks.

So, to be practical, your goal should be to have as little VAT as you possibly can.

How to accomplish this?  Diet and exercise.

For the obese, surgical removal (--or possibly burning off by carefully targeted lasers?--) might be useful.

  --  Saul

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Well, in a very general way, there seems to be a view of how little body fat is too little - this is not specific to VAT, but one wonders if that's a component, where that number would fall. According to this, for men, below 8% body fat is deleterious across all age groups:


I know body builders frequently "cut" to get to like, 5% body fat for competitions, which presumably is not sustainable or advisable outside of these special occasions. Anyhow, in the link they mention Essential Body Fat (as opposed to Storage Body Fat), which should not fall below 3% (for men). How VAT fits into this is an interesting question.


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On 12/31/2019 at 1:51 PM, Sibiriak said:

The Contribution of Age-Related Changes in Adiposity to Inflammation and Disease

(see charts with flattened J-shaped curves for visceral fat and mortality risks, and interesting  group photos of rowers young and old.)


Those same charts appear in the original article cited by Ron (thanks!):

Visceral Fat Is an Independent Predictor of All‐cause Mortality in Men (2006)


Figure 1.  The OR for mortality with increasing visceral fat mass (A) and area (B) after control for age and follow‐up time. The OR for mortality with increasing visceral fat mass (C) and area (D) after control for age, follow‐up time, liver fat, and abdominal subcutaneous fat. The fifth percentile of visceral fat (mass, 0.15 kg; area, 50 cm2) was used as the referent value.

Several things are immediately apparent.   1) There is a minimum amount of VAT in all the curves.   2)  The curves are not U-shaped,  so there is no indication of increased mortality at the lowest end of the visceral fat amount.  3) The beginning of the curves are quite flat,  indicating that the amount of VAT must reach  a certain level before there is any significant increase in mortality risk.

According to the authors of the study:


Our findings suggest that the relationship between visceral fat and mortality is curvilinear. Inspection of Figure 1 reveals that a rather large amount of visceral fat (∼200 cm2 at the L4‐L5 level) accumulation is required before observing a substantially elevated risk of mortality.

This threshold is greater than the level of visceral fat (∼110 to 130 cm2 at L4‐L5) thought to be associated with a disproportionate increase in metabolic risk in moderately aged men ((20)).

It is likely that these observations are consistent. In other words, a longer follow‐up period in our study may have revealed that, at a younger age, our sample of older men had levels of visceral fat in the order of 130 cm2 combined with increased metabolic risk factors. It is well established that visceral fat accumulation increases with advancing age ((22)).


Edited by Sibiriak
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