Educational Forum with Clinical Studies Current Science and Research

November 30, 2010

Obesity. Xanya Sofra Weiss

Filed under: Xanya Sofra Weiss — Tags: — Dr. Xanya @ 10:04 pm

Obesity is not just a cosmetic problem, but it can lead to a lot of health problems and complications. The health problems associated with obesity are diabetes, heart diseases, arthritis, stroke, liver disease, gall stones etc.

Obesity is because of eating too many calories and not getting enough physical activities to burn those calories. Excess calories are deposited in the body as fat.
Obesity increases the risk of several health problems like high blood pressure, insulin resistance, type 2 diabetes, heart diseases, stroke, gout, gallstones, colon cancer, sleep apnea and non-alcoholic fatty liver disease.

High blood pressure:
Blood vessels carry blood from heart to different organs of the body and back to heart. The blood vessels have thick but elastic walls for proper flow of blood. Decrease in elasticity of blood vessel wall increases pressure on blood passing through these vessels. Obesity decreases elasticity of blood vessels causing increase in blood pressure.

Diabetes in obesity:
Insulin is required for entry of carbohydrate into cells from the blood. The carbohydrate in cell is utilized for energy production by the cells. Excess deposition of fat in the body causes insulin resistance, because of which, insulin cannot perform its function and sugar cannot enter into cells and remain in blood. This leads to diabetes or high blood sugar. High sugar in blood leads to complications in various organs like kidney, eyes, blood vessel, and heart.

Atherosclerosis or fatty deposits in blood vessels:
Obesity is associated with increase in levels of bad cholesterol in blood. Increase cholesterol in blood causes atherosclerosis or deposition of cholesterol on the walls of blood vessels. Atherosclerosis reduces the elasticity of blood vessels, narrows blood vessels and decreases blood flow through these vessels. All these changes lead to increased risk of heart disease and stroke.

Heart diseases:
Coronary arteries are the blood vessels that supply blood to heart muscles. Atherosclerosis or fatty deposits in coronary arteries in obesity decreases blood supply to heart muscles. Decreased oxygen supply and blood flow to heart can cause angina (chest pain) and complete blockage of blood flow to heart can cause heart attack.

Stroke or paralysis:
Atherosclerosis in arteries of brain can reduce blood supply to the brain. This decrease in blood flow can result in stroke or paralysis.

Obesity and overweight increases the load on the joints such as the knee, hip and lower back, which can cause the breakdown of cartilage in the joint. Cartilage is a cushion like structure in a joint required for smooth movement of joints. Breakdown of cartilage in obesity results in joint pain and stiffness and other features of osteoarthritis.

A type of arthritis caused by the accumulation of uric acid crystals in joints. Obesity is associated with increased accumulation of these solid crystal-like masses in joints, which causes inflammation and pain.

Sleep apnea:
Overweight and excess fat around neck causes narrowing of airways and leads to sleep apnea. In sleep apnea, person snores heavily and stops breathing for short periods, which results in frequent awakening at night.

Fatty liver disease:
Obesity increases the risk of developing liver disease called fatty liver disease due to accumulation of fat in liver.

Gallbladder disease and gallstones:
Obesity increases cholesterol deposition in gall bladder, which can lead to formation of gallstones.

So, obesity can lead to a lot of health problems and other complications.
For details on role of nutrients in various diseases, please visit Diet for Disease and for information on management of obesity by blocking carbohydrate absorption, please visit
Carbohydrate in Obesity website.

Xanya Sofra Weiss

Xanya Sofra Weiss

The influence of obesity on calf blood flow and vascular reactivity in older adults. Xanya Sofra Weiss

Filed under: Xanya Sofra Weiss — Tags: — Dr. Xanya @ 10:02 pm


To determine whether differences in vascular reactivity existed among normal weight, overweight, and obese older men and women, and to examine the association between abdominal fat distribution and vascular reactivity.


Eighty-seven individuals who were 60 years of age or older (age = 69 ± 7 yrs; mean ± SD) were grouped into normal weight (BMI < n =” 30),” n =” 28),” n =” 29)” p =” 0.038)” p =” 0.001)” p =” 0.006,” r =” -0.44,” r =” -0.37,” r =” -0.36,” p =” 0.001,” r =” -0.32,” p =” 0.002).” bmi =” weight” r =” 0.86″> 0.05) to calf blood flow obtained at rest. BMI was inversely related to the post-occlusive reactive hyperemic calf blood flow (r = -0.25, p = 0.022), and to the absolute change (r = -0.44, p < r =” -0.37,” r =” -0.21,” p =” 0.047),” r =” -0.36,” p =” 0.001)” r =” -0.32,” p =” 0.002)”>

Figure 1. The relationship between body mass index and the percentage change in calf blood flow from rest to post-occlusive reactive hyperemia (r = -0.37, p <>

Figure 2. The relationship between waist circumference and percentage change in calf blood flow from rest to post-occlusive reactive hyperemia (r = -0.32, p = 0.002).

One subject had a percentage change in calf blood flow that exceeded 900%. We used two different approaches to assess whether this data point had an influence on the relationships shown in Figures 1 and 2. In the first approach, we used non-parametric procedures by calculating the Spearman Rank correlation coefficients. The percentage change in calf blood flow remained significantly related to BMI (r = -0.38, p < r =” -0.33,” p =” 0.002),” r =” -0.23,” p =” 0.036),” r =” -0.36,” p =” 0.001)” r =” -0.28,” p =” 0.014)” r =” -0.33,” p =” 0.002)” r =” -0.26,” p =” 0.019)”>

This investigation compared the reactive hyperemic response to three minutes of arterial occlusion in older adults having a wide range in BMI, and determined if calf blood flow differences among normal weight, overweight, and obese older adults persisted after adjusting for confounders, such as age and hypertension. The primary findings were: (1) the obese group had a blunted change in post-occlusive reactive hyperemic blood flow, indicative of impaired vascular reactivity, than the normal weight group, and (2) the difference in vascular reactivity between the obese and normal weight groups remained significant after controlling for age, hypertension and calf skinfold thickness.

The observation that obesity impairs vascular reactivity supports previous studies in young and healthy adults [8,16,21], and extends this finding to obese older adults who are free of overt cardiovascular disease. This suggests that obesity-mediated vascular dysfunction in older adults is due to impairment in endothelial function [8,16]. Our results are further supported by a report that found an inverse correlation between obesity and endothelial-independent vasodilation [22] in a small sample of older adults with diabetes. Collectively, these findings suggest that obesity has a detrimental impact on endothelial function in older adults with and without diabetes.

Besides the negative consequences of obesity on vascular function in older populations, obesity-mediated alterations in endothelial function are evident even in young adults. A lower response in endothelial-dependent vasodilation and forearm blood flow after an infusion of acetylcholine (ACh) is observed in obese, young adults compared to overweight and normal weight young adults [8]. Accumulation of abdominal fat is the primary factor for endothelial dysfunction [21]. Interestingly, endothelial function may be positively altered following a weight loss program. A prospective investigation found ACh-stimulated forearm blood flow improved following a reduction in body size and waist circumference [16]. In speculation, a program designed to decrease adiposity may improve endothelial function in older, obese adults.

The increased prevalence of chronic vascular complications consistently shown in the aging population [23,24] further complicates the association between obesity and endothelial function. The development of endothelial dysfunction and, ultimately, atherosclerosis has specifically been linked to diabetes [25], hypertension [26], and hypercholesterolemia [27], all of which increase in prevalence with advancing age [28]. Additionally, lifestyle behaviors such as physical inactivity and smoking, impair endothelial function and initiate atherosclerotic processes [23,24,29-31]. The lack of control of these co-morbid conditions leaves previous results inconclusive regarding the independent role of obesity in the pathogenesis of endothelial dysfunction. The current investigation attempted to minimize these confounding factors by excluding subjects with cardiovascular disease, diabetes, and a history of smoking during the previous year. Furthermore, vascular reactivity measurements were adjusted for group differences in age, prevalence of hypertension and calf skinfold thickness. These approaches improve the ability to determine the influence of obesity on vascular reactivity.

Finally, subcutaneous body fat, as assessed by the sum of skinfolds, did not show any relationship to blood flow or to vascular reactivity in this population. In contrast, the central distribution of adipose tissue, as assessed by waist circumference, was inversely related to vascular reactivity of these older adults. Taken collectively, these results suggest that visceral adiposity may have a more detrimental influence on vascular reactivity (i.e., endothelial dysfunction) than subcutaneous fat. Our findings are supported by a previous observation that impairment in flow-mediated, endothelium-dependent vasodilation of the brachial artery occurs with visceral obesity, rather than with subcutaneous obesity [32].

One limitation to this study is the cross-sectional design which does not establish a causal link between obesity and impaired vascular reactivity. Intervention and longitudinal studies that track changes in fat mass and vascular reactivity are necessary to better determine their association. Although we normalized the blood flow measures according to subcutaneous fat of the calf, as estimated by the calf skinfold, we did not measure intra-muscular fat. Therefore, it is possible that the difference in blood flow among the groups is partially attributed to differences in intra-muscular fat of the calf. Additionally, the measurement of vascular reactivity by the method of reactive hyperemia assesses the vasodilatory function of both the endothelium and vascular smooth muscle, and therefore is only an indirect assessment of endothelial function. The lack of physical activity measurement is another limitation to this study. Physical activity status is associated with blood flow [24] and endothelial-dependent vasodilatory function [29] and, thus, should be considered in future studies examining the influence of obesity and abdominal fat on vascular reactivity.

Although our investigation minimized confounding factors by excluding for cardiovascular disease and controlling for many primary risk factors of atherosclerosis, we did not adjust for the possible influence of secondary risk factors, such as C-reactive protein or other inflammatory markers [33,34]. Furthermore, a medical history was used to exclude participants with diagnosed cardiovascular disease and diabetes, but those with undiagnosed conditions may not have been identified. That said, the possibility exists that our self-report method of revealing existing disease does allow for an underestimated prevalence of diabetes. Lastly, our assessment of adiposity was limited to BMI and anthropometric measures rather than more precise measurements of body fat and displacement of adiposity.

In conclusion, obesity and abdominal adiposity impair vascular reactivity in older men and women, and these deleterious effects on vascular reactivity are independent of conventional risk factors. Consequently, impaired vascular reactivity may increase the risk for subsequent cardiovascular complications in older, obese adults.

Xanya Sofra Weiss

Xanya Sofra Weiss

New Treatment for Obesity. Xanya Sofra Weiss

Filed under: Xanya Sofra Weiss — Tags: — Dr. Xanya @ 9:59 pm

Obesity is associated with more than 30 medical conditions including Type 2 Diabetes, Coronary Heart Disease, Osteroarthritis, High Blood Pressure, Breast Cancer, Cancers of the Esophagus and Gastric Cardia, Impaired Immune Response. Low Back Pain etc. Selim et al (2008) have shown that Obesity is related to reduced blood flow velocities in the middle cerebral arteries. Laasko et al (1990) has shown that reduced insulin-mediated glucose uptake in human obesity is due to defects in insulin’s action to increase blood flow to these tissues. Laasko et al report that this defect in insulin’s action is a novel mechanism of insulin resistance. Overall, obesity is characterized by decreased blood flow into muscle. The reduced blood flow and/or tissue activity can lead to decreased insulin-medicated glucose uptake, another factor associated with obesity according to Laasko et al (1990). Cheuk-Kwan Sun et al (2003) demosnstrated that obesity is related with reduced portal venus blood flow, and a decrease in overall hepatic perfusion and oxygenation. A clinical study with individuals presenting abnormally clumped Red Blood Cells’ (RBCs) was completed in February 2009 with a device representing the Pacemaker Technology for the Skeletal muscle (PTSM / Ion Magnum – IM). Results (see figure 1) indicate that this technology rapidly and efficiently leads to normalized erythrocytes’ separation at the microscopic level. RBCs separation is crucial for the overall blood flow and timely transport of hormones, antibodies, oxygen and nutrients to the cells, and waste products to the kidneys. Transport of Hormones is a crucial process lipolysis (T3 and Growth Hormone — GF) and muscle hypertrophy (Insulin Growth Factor – IGF-1). Additionally, erythrocyte separation resulting from treatment with the Pacemaker technology for the skeletal muscle appears to have a negative correlation with the number of fungal forms, poikilocytosis, thrombocyte aggregation and bacteria present in the blood prior to the IM treatments, In summary, the erythrocyte separation resulting from treatments with the pacemaker technology for the skeletal muscle enhance hormonal transport including T3 and GH enhances hormonal transport including T3 and GH leading to lipolysis and muscle hypertrophy; 2) RBC;s separation enhances overall level of health by a significant reduction of free radicals. bacteria, fungal forms. etc.; 3) Obesity is characterized by reduced blood flow. PTSM increases RBC’s separation resulting in normalized blood flow. In conclusion, re-establishing normal levels of blood flow will not only help reduce obesity but it will help reduce the risk of heart attack as well as all other disorders associated with obesity. The fact that the Pacemaker Technology for the Skeletal muscle reduces Obesity is shown in a recent clinical study 2009. Five separate clinics from around the world participated in this clinical study . All five subjects that participated in the study showed substantial weight loss, including reduction of visceral fat. Jensen (2008) reports that an upper body/visceral fat distribution in obesity is closely linked with metabolic complications, whereas increased lower body fat is independently predictive of reduced cardiovascular risk. The before and after of subject 3 are shown in figure 2. IM Research, the Pacemaker Technology, London University, UK Xanya Sofra-Weiss, Ph.D

The Pacemaker Technology for the Skeletal Muscle (PTSM) is a voltage driven device, very much like the Pacemaker. However, due to the complexity of the CNS, PTSM is based on a dynamic multi-sine, analogue waveform that was originally tested at the cellular level by Dr. Donald Gilbert, a molecular biologist, in the eighties. After 30 years of research, the IM was electronically engineered by the Co-Inventor of the first Pacemaker (2008) to resonate the motor nerve’s signal of strenuous exercise normally emitted by the brain. Due to its resonance with the biological signal, the PTSM signal spreads throughout the CNS inducing effortless and painless isometric and isotonic muscle contractions. The signal to the nerve ultimately triggers hormonal secretion such as Growth Hormone (GF), Thyroxine (T4) and Triiodothyronine (T3) for lipolysis and Insulin Growth Factor (IGF-1) for muscle hypertrophy.

Xanya Sofra Weiss

Xanya Sofra Weiss

Calcium homeostasis in ageing: studies on the calcium binding protein calbindin D28K. Xanya Sofra Weiss

Filed under: Xanya Sofra Weiss — Tags: — Dr. Xanya @ 9:53 pm

G. Lally , R. L. M. Faull , H. J. Waldvogel , S. FerrarP, and P. C. Emson; 1997

Calbindin D28 K is a neuronal calcium binding protein which may act as a buffer of neuronal calcium. Evidence suggests that disturbance of calcium homeostasis is important in neurodegeneration, possibly via changes in calbindin D28K. Immunoreactivity of calbindin D28 N is compared in Alzheimer’s disease and age-matched controls. The size and number of calbindin D28 K positive neurons in Alzheimer’s disease tissue is reduced. There is also shrinkage of the dendritic tree. Continuing work examines the function of calbindin D28 K using transgenic mice. (J Neural Transm 104:1107-1112)

Xanya Sofra Weiss

Xanya Sofra Weiss

Changes in Calcium Homeostasis during Aging and Alzheimer’s Disease. Xanya Sofra Weiss

Filed under: Xanya Sofra Weiss — Tags: — Dr. Xanya @ 8:55 pm


Several observations indirectly suggest that intracellular calcium regulation may be altered by aging and Alzheimer’s disease. Thus, calcium homeostasis was examined directly in skin fibroblasts from Alzheimer’s patients and compared to cells from normal young and elderly controls. Alterations in both bound and free calcium were noted; cells from Alzheimer’s donors have higher levels of bound calcium but lower concentrations of free intracellular calcium when compared to cells from young and normal aged donors. These changes in calcium homeostasis may be physiologically significant, since processes that require transient elevations of intracellular free calcium, such as cell spreading, decline in the Alzheimer’s cells. In summary, cultured skin fibroblasts from normal aged and Alzheimer’s patients demonstrate deficits in calcium homeostasis and other metabolic processes when compared to cells from young donors.

Xanya Sofra Weiss

Xanya Sofra Weiss

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