The Truth About Fat Burning Foods
The bone marrow is the site of generation of most mature circulating blood cells, including red cells, granulocytes, and monocytes, and the site of early events in B cell maturation. The generation of all blood cells, called hematopoiesis (Fig. 2-9), occurs initially, during fetal development, in blood islands of the yolk sac and the para-aortic mesenchyme, then shifts to the liver between the third and fourth months of gestation, and gradually shifts again to the bone marrow. At birth, hematopoiesis takes place mainly in the bones throughout the skeleton, but it becomes restricted increasingly to the marrow of the flat bones so that by puberty, hematopoiesis occurs mostly in the sternum, vertebrae, iliac bones, and ribs. The red marrow that is found in these bones consists of a sponge-like reticular framework located between long trabeculae. The spaces in this framework contain a network of blood-filled sinusoids lined by endothelial cells attached to a discontinuous basement...
Seborrheic dermatoses and other forms of scaly skin rash may respond to biotin, particularly when taken as part of a complete vitamin B complex in conjunction with essential fatty acids (omega-6 and omega-3 fatty acids). 1 These dermato-logic disorders may be due to impairments of essential fatty acid metabolism in the skin, produced by abnormal biotin metabolism or deficiency.
Other atrophies of small, circumscribed areas of subcutaneous fat layers can appear after a local trauma or prolonged pressure, or at the site of drug (mainly of protein structure) injection. Extractive hormones, e.g. bovine insulin, growth hormone, ACTH, calcitonin, and vasopressin, have been reported to be responsible for this form of fat atrophy at injection sites. Local formation of immunocomplexes, or protein precipitate or activation of complement fractions could induce a local lipolytic response mediated by inflammatory agents, and may explain the zonal loss of subcutaneous fat. Tumour necrosis factor (TNF)-a release induced by insulin may mediate adipocyte atrophy 19 . An asymptomatic, discoid or funnel-shaped depression appears. Microscopic examination of biopsy samples of tissue from atrophic area shows the disappearance of fat cells. A dedifferentiation of fat cells to fibroblast-like cells can be postulated, rather than adipocyte necrosis. In fact, the subcutaneous fat may...
Lipoatrophy Associated with Multiple Symmetric Lipomatosis Launois Bensaude Syndrome or Madelung Collar
There is evidence for a mitochondrial dysfunction in muscle fibres. Levels of respiratory-chain enzyme show a significant decrease of cytochrome-c oxidase, succinic dehydrogenase, and citrate synthase activity 52 . Reduced mito-chondrial enzyme activity could provide the pathogenetic basis of the multisystemic clinical manifestations of MSL. Cultured MSL adipocytes synthesise UCP-1, the selective marker of brown adipocyte, but unlike in normally functioning brown fat cells, UCP-1 gene expression was not significantly induced by noradrenaline. Thus, MSL may be the consequence of a defective noradren-ergic modulation of proliferation and differentiation of brown fat cells 53 .
Those who want to lose weight can do so on this diet by gradually reducing their caloric intake. It is important to take it slow, because drastically reducing your caloric intake can lead to the loss of lean tissue. When you reduce your caloric intake gradually, your body burns fat stores for energy, and does not consume much lean tissue. However, when you cut back drastically, lean tissue eventually is burned in substantial amounts. Not only does this reduce body protein stores, but it also tends to defeat the goal of protein restriction. Total fasting, for exam
Omega-3 oil fish or pills Consumer Reports 2003July 30-32. Bates D, Cartlidge NEF, French JM, et al. A double-blind controlled trial of long chain n-3 polyunsaturated fatty acids in the treatment of multiple sclerosis. J Neurol Neurosurg Psychiatry 1989 52 18-22. Bates D, Fawcett PRW, Shaw DA, et al. Polyunsaturated fatty acids in treatment of Swank RL, Dugan BB. Effect of low saturated fat diet in early and late cases of multiple sclerosis. Lancet 1990 336 37-39. Swank RL, Goodwin J. Review of MS patient survival on a Swank low saturated fat diet. Nutrition 2003 16 161-162. Weinstock-Guttman, Baier M, Park Y, et al. Low fat dietary intervention with omega-3 fatty acid supplementation in multiple sclerosis patients. Prostaglandins Leukotrienes Essential Fatty Acids 2005 73 392-404.
The two essential fatty acids for humans are linoleic and linolenic acid. Because mammalian cells lack the enzymes necessary for their synthesis, these two polyunsaturated fats must be obtained from dietary sources and are therefore termed essential fatty acids (EFAs). Linoleic acid is a member of the omega-6 fatty acid family, whereas linolenic acid is part of the omega-3 fatty acid group. The omega-3 or omega-6 designation (n-3 and n-6 notation is also used) refers to the distance of the first unsaturated bond from the methyl end of the fatty acid.
For people with chronic ailments that may benefit from increasing omega-3 intake, supplements are usually inthe range of 2-4g day. 2. For people with chronic ailments that may benefit from increasing omega-3 intake, supplements are usually inthe range of 2-4g day. Omega-3 High doses of GLA, EPA, and DHA should always be taken with additional vitamin E. As body stores of these polyunsaturated fats increase, additional vitamin E antioxidant protection is required. When taking omega-3 and omega-6 fatty-acid supplements, additional vitamin E (30-100 mg) and selenium (50100 ug) is recommended.
Dietary recommendations for cancer patients are currently based on reference values for the diet of a healthy person, like those established by the German Society of Nutrition (22). As there is evidence that certain nutrients (e.g., omega-3 fatty acids) influence the growth and metabolism of cells, the condition and regeneration of tissues, and also the modulation of immune defenses, attempts have been made to improve the nutritional state of cancer patients by means of such substances (77, 78). However, clear recommendations are not yet available.
The subcutaneous fat (panniculus adiposus) is located below the reticular dermis and extends to the superficial fascia. The tissue is divided into lobules composed of aggregates of adi-pocytes (fat cells, lipocytes) separated by a meshwork of fibrous septae (trabeculae). The fibrous septae extend down from the reticular dermis and house small- to medium-sized arteries, arterioles, venules, lymphatics, and nerves. An arteriole supplies the center of each lobule with drainage to peripheral venules in the fibrous septae. Lymphatics are not present within the lobules. Each adipocyte is supplied by capillaries. Therefore, venous processes are
In the second half of pregnancy, protein needs almost double - the average woman requiring 40-50 g day before pregnancy now requires 70-90 g day.4 The choice of dietary fat is important. A pregnant woman's diet should be rich in the omega-3 fatty acids, eicosapenta-noic acid (EPA), and docosahexanoic acid (DHA). These fatty acids are important components of the developing baby's central nervous system and eyes. Because most of the cells in the central nervous system are formed during pregnancy and the first year after birth, ample intakes of EPA and DHA are vital during this period.5 Although adults are able to synthesize some EPA and DHA from li-nolenic acid (see pp.89), the fetus cannot because the necessary metabolic pathways have not fully developed. These fatty acids need to be supplied to the fetus by the mother.
The differences found between body weight and cellular mass are due either to an excess of extracellular water or to fat deposits. Fat is subject to variations not synchronous with those of the cellular mass, related to genetic factors (initial number and size of fat cells) and to hormonal causes, i.e. leptin, lipoprotein lipase (LPL), estradi-
Ent in the milk are derived directly from the maternal diet. Vegetarians produce milk with greater amounts of the fatty acids present in plant foods. Because EFAs (particularly li-nolenic acid and the omega-3 fatty acids EPA and DHA) (see pp.89) are vital for the developing nervous system of the newborn,4 nursing mothers should consume generous amounts. Omega-3 fatty acids
Even though the total fat mass determines the plasma pool of FFA and thereby the FFA flux from adipose to non-adipose tissue (Lewis et al. 2002), there are differences in the relationship of subcutaneous and visceral fat depots to features of peripheral and hepatic insulin sensitivity (Misra et al. 1997). Visceral fat cells are more sensitive than subcutaneous fat cells to the lipolytic effect of catecholemines and less sensitive to the antilipolytic and fatty acid re-esterification effects of insulin (Kahn & Flier 2000). Furthermore, the venous effluent of visceral fat depots leads directly into the portal vein, resulting in greater FFA flux to the liver. This makes the visceral fat depots more efficient than subcutaneous fat in influencing the carbohydrate metabolism in the human body (Kissebah 1996).
Adipsin, which is identical to complement factor D and synthesised by fat cells, is profoundly deficient in mice with genetic and hypothalamic obesity 48 . In humans, circulating concentrations of adipsin tend to correlate positively with the degree of adiposity, being mildly elevated in obese individuals and mildly reduced in those with total lipoatrophy cachexia related to AIDS 49 .
During fasting, fat cells supply fuels for other parts of the body. Because fats are insoluble and fatty acids have only a limited solubility, fat cells convert fatty acids into soluble, circulating fuels called ketone bodies (Fig. 13.8) (the word ketone means any chemical containing a carbon atom with single bonds to two other carbons and a double bond to an oxygen). The fundamental ketone body is acetoacetate, which the liver synthesizes from acetyl-CoA. Acetoacetate is then reduced to 3-hydroxybutyrate. These two molecules are important circulating fuels in mammals. Heart muscle, for instance, prefers ketone bodies to glucose as a fuel source.
Linoleic acid (LA) is a member of the family of omega-6 (T-6 or n-6) fatty acids a-linolenic acid is an omega-3 (T-3 or n-3) fatty acid. These terms refer to characteristics in the chemical structure of the fatty acids. Other omega-6 fatty acids can be manufactured in the body using linoleic acids as a starting point. These include gamma-linoleic acid (GLA), dihomo-gamma-linoleic acid (DHGLA), and arachidonic acid (AA). Similarly, other omega-3 fatty acids that are manufactured in the body using a-linolenic acid as a starting point include eicosapentaenoic acid (EPA) and docosa-hexaenoic acid (DHA). Many fatty acids are sold as supplements in natural food and health stores, and these ingredients are commonly featured on the label. Among the significant components of cell membranes are the phospholipids, which contain fatty acids. The type of fatty acids in the diet determines the type of fatty acids available to the composition of cell membranes. A phospholipid made from a saturated...
Fats (lipids) and fatty acids, in a manner similar to many organic chemicals, are represented by combinations of various carbon, oxygen, and hydrogen elements that are linked together by one or two bonds. Each carbon has four binding sites. In the carbon chain, two sites will be taken up by other carbons (i.e., the two adjacent carbons on the chain). In a saturated fat, the other two sites are taken up by hydrogen atoms. Saturated fats are typically solid at room temperature, such as lard and butter, and are generally of animal origin. Saturated fats are generally burned as fuel by our bodies. Unsaturated fats have two adjacent carbons held together by a biochemical double bond. These fats are generally liquid at room temperature and are of plant origin (olive oil, corn oil, etc.). Unsaturated fats can be classified as omega three fatty acids (or T-3 or n-3) or omega six fatty acids (or T-6 or n-6), depending on the location of the double bond relative to the end of the chain. These...
Differences in body fat arise at puberty when young women begin to store fat in their stomach, buttocks, and legs. This, in addition to skeletal differences, gives women's bodies their curvy shape. Men usually carry their fat in the abdomen. Overall, women have about 10 more body fat then men, which is necessary to maintain fertility. As we discussed in Chapter 2, body fat is required for female fertility because a hormone called leptin, secreted by fat cells, tells the brain if there are enough fat stores to support a pregnancy. When a female does not have enough body fat, the hormones that regulate menstruation are blocked and menstruation ceases. Lack of menstruation can be permanent and results in sterility and bone damage. Excessive exercise or starvation that leads to the cessation of menstruation, called amenorrhea, causes permanent damage when the estrogen that normally increases prior to ovulation is not produced.
In fact, it is impossible to determine a person's gender on the basis of their body-fat percentage. If all you knew about a person was that their body-fat percentage was 18 , you would have no way to predict whether they were male or female. In the same way, it would be very difficult to predict a person's body-fat percentage solely on the basis of his or her gender. The range of body-fat percentages for normal women shows a 20 difference from lowest to highest for men the range varies by 26 . However, the average difference between men and women is only 7 . As is often the case when we try to study differences between various groups, the differences within a group are greater than the differences between two groups.
Suboptimum micronutrient intake during childhood can be a cause of learning disability.11 Deficiencies of iron, magnesium, iodine, and zinc can reduce learning ability, and even marginal deficiencies can have subtle adverse effects. For example, moderate iron deficiency during early childhood and adolescence can decrease IQ and mental development.12,13 Along with minerals and vitamins, a rich supply of essential PUFAs is important. The omega-3 fatty acids (found in fish and shellfish) are critical to the formation of neurons and their supporting tissues in the brain during early childhood.14 Food sensitivities can play a role in learning disabilities in children, particularly sensitivities to food ad-
Placebo-controlled study on the malnourished group. Fourteen patients received daily oral BCAA supplementation (12 g day) or a placebo in random order in a cross-over trial for 6 months. Lower plasma levels of BCAA and lower protein and caloric intakes were found in the malnourished group as compared to the well-nourished group. In BCAA-treated malnourished patients, anorexia and poor oral protein and calorie intakes improved within a month, concomitant with the improvement of plasma BCAA levels over the values in well-nourished patients. After 6 months of BCAA supplementation, anthropometric indices (body fat percentage, lean body mass) showed a statistically significant increase and mean plasma albumin concentration increased from 3.3 g dl to 3.9 g dl. After changing BCAA for a placebo, spontaneous oral food intake decreased, but the favourable nutritional status persisted for the next 6 months. In 14 patients initially treated with placebo, no significant changes in nutritional...
Complete formula emphasizing thiamin (B1) and vitamin B6 Omega-3 fatty acids (1-2 g EPA as fish-oil capsules) plus GLA as 1-2 g evening primrose oil Balanced supplement containing ample amounts of zinc and magnesium PUFA metabolism may be abnormal in children with ADHD,23 and deficiencies of omega-3 and omega-6 fatty acids are found in many children with ADHD23
N-3 fatty acids, mainly from fish oils, interfere with the cyclooxygenase (PGE2 production) and lipooxygenase metabolic pathways. They also inhibit cytokine synthesis and activity 151, 152 . Dinarello 153 and Endres 154 found that N-3 fatty acids improved food intake in rats with IL-1-induced anorexia. Tisdale and Dhesi also reported that using omega-3 fatty acids stopped the weight loss in an experimental cachexia model 155 . While the role of N-3 fatty acids in the treatment of cancer cachexia remains unclear 156 , their potential role in the treatment of cancer cachexia is promising 157,158 .
One of the mechanisms by which stress and glucocorticoids are thought to influence neuronal survival and function is by reducing the energy capacity of neurons (see ref. 6). Glucocorticoids are known to decrease the uptake of glucose in peripheral tissues, including fat cells and fibroblasts, and a similar effect is observed in the brain (Fig. 2). The mechanisms responsible for the decreased glucose uptake include both transcriptional and posttran-scriptional modifications. Long-term exposure of adipocytes to glucocorti-coid decreases the expression of the glucose transporter and thereby decreases the ability of cells to accumulate glucose (27). This occurs via glucocorticoid
All cells need fatty acids for membrane lipids. Fat cells make large amounts of fat (triacyl-glycerols) in times of plenty. The basic machinery is a multienzyme complex (in bacteria) or a multidomain protein (in eukaryotes) that uses the substrate acetyl-CoA. In both cases the growing fatty acid chain is not released it swivels from enzyme to enzyme or domain to domain in the array, adding two carbons for each complete cycle until the limiting length of 16 carbons is reached The product, palmitic acid, is then released. Although the reactions look similar (Fig. 13.12), the process is not a reversal of j oxidation (page 290). It uses entirely different enzymes, takes place in the cytosol rather than in the mitochondria, and is separately regulated. Like much of biosynthesis it is reductive, and the reducing power comes not from NADH but from the closely related dinucleotide NADPH.
Omega-3 fatty acids Fig. 5.1 Omega-3 fatty acids and psoriasis. 28 subjects with stable chronic psoriasis were given 1.8 g omega-3 fatty acids or placebo for 12 weeks. In the treatment group, itching, scaling, and erythema were all significantly reduced at 8 and 12 weeks compared with placebo. The percentage of surface area affected was also decreased by treatment with omega-3 fats (7 vs. 12 , treatment vs. control) (Adapted from Bittiner SB, et al. Lancet. 1988 1 378)
For the vast majority of epilepsy patients, no evidence links dietary changes and either improvement or exacerbation of seizure activity. Many anecdotal reports arise from individual patients or families that certain foods (e.g., those with high sugar content) or additives (e.g., aspartame) can trigger seizures. Little evidence supports these associations when scientifically studied (8,9). Similarly, some patients with epilepsy take antioxidants and free radical scavengers, such as omega-3 fatty acids and vitamin E (10,11). Although some evidence suggests that this class of compounds may reduce cancer risk and slow the progression of neurodegenerative disorders such as Alzheimer's
All the major molecules produced by murine fat cells (e.g. leptin, adiponectin, TNF-a, angiotensinogen, PAI 1, resistin, adipsin) are also produced by human adipocytes. Also in our species, regulation of the amount of fat tissue depends on the energy balance. If there is a positive balance, adult individuals exhibit an increase in adipocyte size, which, upon attainment of a critical size, will induce the development of new fat cells (see also 'Vessels and Nerves').
The primary function of mitochondria is generation of energy in the form of ATP for molecular and cellular activities. Sources for mitochondrial energy generation are fatty acids and glycogens, or glucose polymers. Fatty acids are a more efficient form than glycogen for energy generation. The oxidation of fatty acids can generate energy 6 times as much as that of an equal amount of glycogen. Fatty acids are mainly stored in fat cells,
Effect of low saturated fat diet in early and late cases of multiple sclerosis. Lancet 1990 336 37-39. 3. Swank RL, Goodwin J. Review of MS patient survival on a Swank low saturated fat diet. Nutrition 2003 16 161-162. 13. Weinstock-Guttamn B, Baier M, Park Y, et al. Low fat dietary intervention with omega-3 fatty acid supplementation in multiple sclerosis patients. Prostaglandins Leukotrienes Essential Fatty Acids 2005 73 392-404.
When the energy balance is positive, the adipose organ prevalently undergoes an increment in its white component. White adipocytes become hypertrophic and subsequently hyperplastic (likely due to a close causal relationship). In fact, it has been suggested that adipocytes are unable to expand beyond a given maximum volume, or 'critical size', which is genetically determined and specific for each depot 77 . Adipocytes that have reached the critical size trigger an increase in cell number 78-80 . In a recent review, Hausman et al. 81 , after considering the evidence for this theory, conclude that not only paracrine factors, but also circulating factors as well as neural influences may play a large role in regulating adipose tissue development and growth. They suggest that in the development of obesity, enlarged fat cells produce and release proliferative paracrine factors as internal controllers of preadipocyte proliferation, and that their proliferative response is modulated by neural...
Cholesterol plasma levels are part of the syndrome. Total cholesterol levels are not constantly increased, but occasionally can be remarkably high 25 (Table 3). Muscle mass, evaluated by DEXA, is preserved on even increased compared with age-, sex- and BMI-matched subjects. The increase in resting energy expenditure is related to the higher fat-free mass body mass ratio. Two subtypes of CGLD have been identified and are distinguished according to the mode of inheritance 26-29 . Type 1 CGLD is related to an autosomal recessive genetic defect in AGPAT2 isoform. This enzyme, involved in the biosynthesis of triglycerides and phospholipids, is expressed at high levels in adipose tissue. Thus, a defect in AGAPT function may reduce triglyceride synthesis in fat cells. Type 2 CGLD is related to an autosomal recessive involvement of seipin, a protein of unknown function 30 . Mutation of the seipin gene has been reported to cluster in a large consanguineous pedi-
As discussed in Chapter 21, the ketogenic diet consists of high fat and low protein, low carbohydrate foods. The goal of the diet is twofold by forcing the patient to burn fat as fuel instead of carbohydrates, by-products known as ketone bodies (such as acetone) are produced. As a result, an acidic environment is created in the patient by metabolic aci-dosis. This diet can be beneficial, especially if it can be shown that the patient was previously in an alkaline state or had alkalosis (7).
The expression of the proinflammatory cytokine IL-6, like that of TNF-a and IL-8, is increased in human fat cells from insulin-resistant individuals, and IL-6 is also associated with the insulin resistance of obesity and type II diabetes 73 . Interestingly, TNF-a markedly increases IL-6 mRNA and protein secretion. Chronic IL-6 treatment selectively impaired hepatic insulin signalling in vivo, further supporting a role for IL-6 in hepatic insulin resistance. IL-6, like TNF-a, exerts long-term inhibitory effects on the gene transcription of IRS-1, glucose transporter-4 (GLUT-4) and PPARy. Moreover, IL-6 reduced GLUT-4 mRNA and insulin-stimulated glucose transport in vivo 74 . IL-6 also decreased refeed-ing-dependent glucokinase mRNA induction and reduced insulin sensitivity. This decrease was characterised by a reduction in tyrosine phospho-rylation of IRS-1 and a decreased association of the p85 subunit of phosphatidylinositol 3-kinase with IRS-1 in response to physiological insulin...
As most fat cells and pericytes) assists in leukocyte adhesion and trafficking (19). VAP-1 is upregulated during inflammation (20). It exhibits enzymatic properties that lead to production of oxidative substrates, promulgating EC destruction and leukocyte recruitment (21). Transmigration across the endothelium also involves junctional molecules, such as platelet-endothelial (PE)CAM-1, DNAM-1 and ZO-1 (22,23). As the inflammation ensues, EC vasomotor regulatory functions and antithrombotic properties are further lost. Specifically, activated EC over-express tissue factor, ET-1, and AT-II. This is associated with further downregulation of vasodilators, NO, and PGI2. Engagement of cell surface receptors transduces intra-cellular signals for nuclear gene expression via activation of transcription factors such as NF-kB. Leukocyte activation enhances secretion of proinflam-matory cytokines and chemokines. Chemokine release, such as MIF, M-CSF, MCP-1, IL-8, GRO, and MIP-1, leads to increased...
Warm exposure entails a reduction of the orthosympathetic stimulus, resulting in BAT inac-tivation. Morphologically, this corresponds to a transformation of brown fat cells into cells similar to white adipocytes. During this transformation, we have observed a reduced genic expression of UCP1 and increased genic expression of leptin 55 . This suggests that such morphological transformation is accompanied by a new functional situation, with adipocytes losing their thermogenic ability and acquiring the properties of white fat cells, including production of such an important hormone as leptin. This is in line with the observation that classic multilocular brown adipocytes subjected to adrenergic stimulation express UCP1 but not leptin 56, 55 , whereas cold exposure and sympathetico-mimetic drugs reduce leptinaemia 57 and induce the transformation of white into brown adipocytes 58 (see below 'Transdifferentiation').
Transdifferentiation is a biological phenomenon by which a differentiated cell turns phenotypically and functionally into a differentiated cell of another type without undergoing dedifferentiation 64 . We believe that brown and white adipocytes can transdifferentiate into one another in the adipose organ. We report some data providing evidence for physiological transdifferentiation of white into brown fat cells. 'Whereas in the opinion of several researchers the presence of UCP1 is a brown adipocyte hallmark, in our view it is merely a cellular feature that subserves the main function of BAT however, brown adipocytes do not consistently express it, and in some conditions in which they do not do so, they assume the appearance of white fat cells. For instance, in an animal maintained above its thermoneutral temperature (see 'Warm Exposure'), the BAT-activating adrenergic stimulus is off brown adipocytes thus undergo a morphological transformation they become unilocular and lose the...
Lipid administration has little influence on nitrogen loss if it is not supplemented with glucose and proteins. Lipids must be prescribed to avoid deficits in essential fatty acids. New, energetic substrates, such as polyunsaturated omega-3 fatty acids (PUFAs), ornithine-ketoglutarate acid (OKGA), medium-chain triglycerides (MCT), short-chain fatty acids (SCFAs), and glutamine are suggested in order to modulate the different stages A reduced supply of n-6 PUFAs and an increased supply of omega-3 fatty acids (m-3FAs) may reduce the inflammatory cascade of cytokine production. This effect seems to be due to eicos-apentaenoic acid (EPA), C20 5, n-3 and docosa-hexaenoic acid (DHA), C22 6, n-3, the main component of fish oil that decreases plasma triglycerides and VLDL while increases levels of LDL-cholesterol. In contrast to other fatty acids of the n-3 and n-6 series, EPA is a direct suppressant of lipid mobilisation factor in both in vitro and in vivo studies it also counteracts weight...
In psoriasis, metabolism of essential fatty acids (EFAs) in the skin is abnormal. Production of EPA and DHA, the omega-3 fatty acids derived from dietary linolenic acid (see pp.89) is impaired (see Fig. 5.1 ).12 Skin synthesis of GLA from linoleic acid is also abnormal. To provide ample polyunsaturated fatty acids, regular consumption of high-quality, cold-pressed nut and seed oils is important. The diet should also be low in saturated fat and hydrogenated fat.13 Vegetarian diets can sometimes dramatically improve psoriasis. They tend to be low in protein, which can aggravate the condition, and high in EFAs. Food sensitivities should be determined as they may promote psoriasis - in some cases careful food-elimination diets can lead to dramatic improvement of the condition (see pp.205). Alcohol consumption can aggravate psoriasis in certain individuals.
A careful elimination diet (see pp.205) can identify food sensitivities that trigger eczema.17 The most common offending foods are milk, eggs, fish, cheese, nuts, and food additives. Cold-pressed nut and seed oils are high in beneficial EFAs important for skin health and should be consumed regularly. Disturbances in fatty acid metabolism in the skin can produce or aggravate eczema impaired production of omega-3 fatty acids and GLA can increase inflammation in the skin (see pp.89).18
Bined with a high intake of saturated fat, low Fig. 5.9 Omega-3 fatty-acids in hypertension. 156 hypertensive adults were treated for 10 weeks with 5.1 g day of omega-3 fatty acids (EPA and DHA). The mean systolic blood pressure decreased by 4.6 mm Hg and the diastolic pressure by 3.0 mm Hg in the group receiving the fish oil. (From Bonaa KH, et al. N EnglJ Med. 1990 322 795) Fig. 5.9 Omega-3 fatty-acids in hypertension. 156 hypertensive adults were treated for 10 weeks with 5.1 g day of omega-3 fatty acids (EPA and DHA). The mean systolic blood pressure decreased by 4.6 mm Hg and the diastolic pressure by 3.0 mm Hg in the group receiving the fish oil. (From Bonaa KH, et al. N EnglJ Med. 1990 322 795)
The use of low-calorie fat replacers in foods facilitates reductions in the energy density of the diet. However, since fat confers a number of important quality attributes, it is critical that such foods be highly palatable. When all or part of the fat is replaced, the foods must have comparable rheological and sensory-quality attributes to the original high-fat food. Textural properties are particularly important since fat has a pronounced impact on texture, mouthfeel, and hence eating quality. Therefore, in addition to lowering the calorie density, an acceptable fat substitute must have the appropriate functional properties, such as heat stability, emulsification, aeration, lubricity, spreadability, texture, and mouthfeel (Lukacova and Karovicova, 2003 Silva, 1996).
Triacylglycerols are stored within specialized fat cells in the body. Most fat cells are composed of a droplet of lipid surrounded by a thin layer of cytoplasm with a nucleus and a few mitochondria. The resulting tissue is white in color and simply releases or stores fatty acids in response to the needs of the organism. This is the kind of fat that is typically found around our kidneys and under the skin. A second kind of fat is found in babies. Brown fat cells not only have stored triacylglycerols but are also rich in mitochondria, the cytochromes of the mitochondria giving the brown color. Brown fat is a heat-generating tissue. A channel selective for H+ called thermogenin is found in the inner mitochondrial membrane. As fast as the electron transport chain pushes H+ ions out of the mitochondrial matrix, they flow through thermogenin back down their electrochemical gradient into the matrix. In other cells this flux would only occur through ATP synthase and would be tightly coupled...
Healthy Fat Loss For A Longer Life
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