(This is NOT a picture of me! Picture was from Wikipedia.)
Visceral fat (a.k.a. belly fat and love handles) is a response to an energy deprivation. Energy deprivation, such as a glucose deprivation, shifts the body to store fat rather than to utilize the energy. Visceral fat has been an adaptation to reduce starvation.
It's easy to gain and lose visceral fat. During starvation or fasting, the first place which fat is burned is in the abdominal area.
Why does visceral fat disappear so quickly? It is because it's intended to be stored as energy, 'rather like a squirrel hiding nuts'. says Dr Haslam. (Source)
The reverse is also true. Fat is easily gained in the abdominal area.
Evolutionarily, this makes sense. Animals who are susceptible to starvation tend to store visceral fat. This is in contrast to subcutaneous fat, which is to provide insulation. Unlike subcutaneous fat which is located everyone, abdominal fat is located in the abdominal area, which also happens to be the center of mass for the organism. Thus, an animal which stores fat in the abdominal area doesn't suffer from impaired mobility as if it stores the fat as subcutaneous fat.
Thus, it's plausible to hypothesize that preventing hypoglycemia (a state of energy deficiency) would reduce visceral fat.
A few simple ways could help to prevent hypoglycemia. There are many ways to regulate blood sugar, which include eliminating polyunsaturated fats (including eliminating fish oil) and supplementing with aspirin and niacinamide. Yet another one is blood donation. We will emphasize blood donation here.
First, there are a few controlled studies demonstrating that blood donation improves blood sugar levels.
Low iron status and enhanced insulin sensitivity in lacto-ovo vegetarians
Nancy W. Hua1,2, Riccardo A. Stoohs3 and Francesco S. Facchini1,2,3*
1Department of Medicine, Division of Nephrology, San Francisco General Hospital, San Francisco, CA, USA
To test whether or not Fe status might modulate insulin sensitivity, body Fe was lowered by phlebotomy in six male meat-eaters to levels similar to that seen in vegetarians, with a resultant approximately 40 % enhancement of insulin-mediated glucose disposal ðP ¼ 0:0008Þ:
Blood Letting in High-Ferritin Type 2 Diabetes
Effects on Insulin Sensitivity and Cell Function
Jose´ Manuel Ferna´ndez-Real,1 Georgina Pen˜ arroja,2 Antoni Castro,2 Fernando Garcı´a-Bragado,2
Ildefonso Herna´ndez-Aguado,3 and Wifredo Ricart1
A statistically significant increase in insulin sensitivity was observed in the blood-letting group
Iron Depletion by Phlebotomy Improves Insulin Resistance in Patients With Nonalcoholic Fatty Liver Disease and Hyperferritinemia: Evidence from a Case-Control Study
Luca Valenti, M.D.,1 Anna Ludovica Fracanzani, M.D.,1 Paola Dongiovanni, Ph.D.,1
Elisabetta Bugianesi, M.D.,2 Giulio Marchesini, M.D.,3 Paola Manzini, M.D.,4 Ester Vanni, M.D.,2
and Silvia Fargion, M.D.1
Baseline ferritin levels were associated with body iron stores (P < 0.0001). Iron depletion produced a significantly larger decrease in insulin resistance (P = 0.0016 for insulin, P = 0.0042 for HOMA-R) compared with nutritional counseling alone, independent of changes in BMI, baseline HOMA-R, and the presence of the metabolic syndrome. Iron depletion was more effective in reducing HOMA-R in patients in the top two tertiles of ferritin concentrations (P < 0.05 vs controls), and in carriers of the mutations in the HFE gene of hereditary hemochromatosis (P < 0.05 vs noncarriers).
Besides improved blood sugar, blood donation has been shown to have a significant reduction on blood pressure as well. In a 2012 study of subjects who donated 550-800 ml of blood, the phlebotomy group had significantly decreased blood pressure.
[Systolic blood pressure] decreased from 148.5 ± 12.3 mmHg to 130.5 ± 11.8 mmHg in the phlebotomy group, and from 144.7 ± 14.4 mmHg to 143.8 ± 11.9 mmHg in the control group (difference -16.6 mmHg; 95% CI -20.7 to -12.5; P < 0.001). No significant effect on HOMA index was seen. With regard to secondary outcomes, blood glucose, HbA1c, low-density lipoprotein/high-density lipoprotein ratio, and HR were significantly decreased by phlebotomy. Changes in BP and HOMA index correlated with ferritin reduction.
Among women, iron supplementation was significantly associated with higher waist circumference, higher blood pressure, high fasting glucose, and impaired glucose tolerance.
Iron-supplement users (n = 212/1000) showed significantly higher values of prepregnancy body mass index (BMI), actual BMI, waist circumference, blood pressure, fasting glucose, Homeostasis-Model-Assessment-Insulin-Resistance, and lower high-density lipoprotein-cholesterol than nonusers. The prevalence of GDM (70.8% vs 44.4%), hypertension (25.9% vs 9.8%), metabolic syndrome (25.9% vs 10.4%) was significantly higher in the former with a 2- to 3-fold-increased risk at multiple regression analyses. Most glucose values of the oral glucose tolerance test were significantly higher in iron supplemented women, both in GDM and normoglycemic individuals.
Besides metabolic syndrome, iron intake was associated with obesity, as well.
The relationship between iron stores and obesity in menstruating women was studied in 20 obese and 20 nonobese women matched for age and contraception. Although no difference was observed in serum iron or total-iron-binding capacity, the obese group showed significantly higher hemoglobin (137 +/- 9 vs 10 g/L, mean +/- SD; P less than 0.01), hematocrit (0.41 +/- 0.02 vs 0.39 +/- 0.03, P less than 0.05), and serum ferritin concentrations (48.0 +/- 44.3 vs 25.8 +/- 19.5 micrograms/L, P less than 0.05). There was no difference between obese and nonobese women in either the menstrual-cycle interval or the duration of the menstrual flow. Iron intake was significantly higher in the obese group (15.9 +/- 2.9 vs 14.1 +/- 2.9 mg/d, P less than 0.05). These results suggest that obese menstruating women are at low risk of depleting iron stores, possibly because of high iron intake. Iron-fortification programs might thus be undesirable in such subjects.