Association of time of obesity onset with comorbidities in treatment-seeking men and women with severe obesity.

OBJECTIVES: Early obesity onset is a risk factor for specific comorbidities in adulthood, but whether this relationship is present in men and women with severe obesity is unknown. This study aimed to examine whether obesity onset in childhood or adolescence, as compared with adulthood, is associated with higher odds of comorbidities in men and women with severe obesity. METHODS: A cross-sectional study of treatment-seeking men and women with severe obesity attending a tertiary care centre in Norway, from 2006 to 2017, was performed. RESULTS: A total of 4,583 participants (69.13% women) were included. Almost all men (99.69%) and women (99.18%) suffered from ≥1 comorbidities. Compared with women, men were older (mean [SD]) (45.54 [12.14] vs. 42.56 [12.00] years, p < 0.001) and had higher body mass index (44.06 [6.16] vs. 43.39 [5.80] kg m-2, p < 0.001). The most prevalent comorbidities were non-alcoholic fatty liver disease, dyslipidaemia and hypertension among men and dyslipidaemia, non-alcoholic fatty liver disease and joint pain among women. After current age and body mass index were adjusted, childhood onset of obesity (0-11 years), compared with adult onset (>20 years), was associated with lower odds (OR [95% CI]) of obstructive sleep apnoea (OSA) in men (0.69 [0.53, 0.91], p < 0.01) and higher odds of OSA (1.49 [1.16, 1.91], p < 0.01) in women, and the interaction was significant (p < 0.01). Childhood onset of obesity was also associated with higher odds of coronary heart disease in men (1.82 [1.15, 2.89], p = 0.01) and type 2 diabetes in women (1.25 [1.01, 1.54], p = 0.04). CONCLUSION: Childhood onset of obesity was associated with higher odds of coronary heart disease in men and OSA and type 2 diabetes in women, but with lower odds of OSA in men.

Lipid composition of hepatic and adipose tissues from normal cats and from cats with idiopathic hepatic lipidosis.

The purpose of this study was to characterize the lipid classes in hepatic and adipose tissues from cats with idiopathic hepatic lipidosis (IHL). Concentrations of triglyceride, phospholipid phosphorus, and free and total cholesterol were determined in lipid extracts of liver homogenates from 5 cats with IHL and 5 healthy control cats. Total fatty acid composition of liver and adipose tissue was also compared. Triglyceride accounted for 34% of liver by weight in cats with IHL (338 +/- 38 mg/g wet liver) versus 1% in control cats (9.9 +/- 1.0 mg/g wet liver, P < .001). The mass of cholesterol ester was significantly higher in triglyceride-free (TG-free) liver from cats with IHL (741 +/- 340 micrograms/g TG-free wet liver) compared to healthy cats (31 +/- 11 micrograms/g TG-free wet liver, P < .05). Total fatty acid composition of hepatic tissue in the 2 groups differed; palmitate was higher (19.5 +/- 1.1% of total fatty acids in cats with IHL versus 9.2 +/- 2.7% in controls, P < .05), stearate was lower (8.5 +/- 0.8% versus 16.8 +/- 1.1%, P < .05), oleate was higher (41.2 +/- 1.6% versus 31.1 +/- 1.8%, P < .05), and arachidonate was lower (1.2 +/- 0.2% versus 6.0 +/- 0.9%, P < .05). The total fatty acid composition of adipose tissue also differed between the 2 groups; palmitate was higher (26.2 +/- 1.2% in cats with IHL versus 21.3 +/- 0.6% in controls, P < .05), total monounsaturated fatty acids were higher (48.4 +/- 1.0% versus 45.0 +/- 0.8%, P < .05), linolenate was lower (13.3 +/- 1.6% versus 17.5 +/- 0.9%, P < .05), total (n-6) fatty acids were lower (13.8 +/- 1.38% versus 18.4 +/- 0.83%, P < .05), linolenate was lower (0.2 +/- 0.04% versus 0.7 +/- 0.06%, P < .06), and total (n-3) fatty acids were lower (0.3 +/- 0.02% versus 1.3 +/- 0.32%, P < .05). The fatty acid composition of both liver and adipose tissue was similar for stearate, oleate, linoleate, and linolenate in cats with IHL. These results support the hypothesis that the origin of hepatic triglyceride in cats with IHL is the mobilization of fatty acids from adipose tissue.

Incorporation of dietary n-3 fatty acids into the fatty acids of human adipose tissue and plasma lipid classes.

The consumption of n-3 fatty acids from seafood has been related to a lower incidence of coronary artery disease. Adipose tissue composition has served as a biological marker of chronic ingestion of many dietary polyunsaturated fatty acids. However, the incorporation of n-3 fatty acids into the fat depots has not been studied in humans. Daily dietary supplementation with > or = 10 g n-3 fatty acids from fish oil for > 12 mo resulted in significantly greater 20:5n-3, 22:5n-3, and 22:6n-3 concentrations in fatty acids of adipose tissue, and a greater 20: 5n-3 fatty acid content in plasma lipid classes (cholesterol esters, phospholipids, and free fatty acids) of supplemented subjects compared with nonsupplemented control subjects. Combined values for all subjects indicated that fatty acid concentrations of n-3 plasma lipid classes, including 20:5n-3, 22:5n-3, 22:6n-3, and total n-3, significantly correlated with corresponding concentrations of fatty acids in adipose tissue. These findings indicate that the long-term ingestion of large amounts of n-3 fatty acids in humans resulted in their incorporation into the adipose tissue fatty acids. Incorporation of the fatty acids into adipose tissue warrants consideration for use in clinical studies requiring precise documentation of long-term n-3 fatty acid consumption.

Postnatal deficiency of omega-3 fatty acids in monkeys: fluid intake and urine concentration.

Previous studies demonstrated increased fluid intake in rhesus monkeys exposed to combined prenatal and long-term postnatal (PRE+POST) dietary deficiency of omega-3 fatty acids. Here we determined the effect of dietary deficiency in omega-3 fatty acids occurring only prenatally (PRE) or only postnatally (POST). Water intake over 24 hours, water intake in 15-minute tests, and excretion of combined urine and feces over 24 hours were all about twice as great in POST as in PRE monkeys. Neither group preferred or avoided salt solutions compared to water in two-bottle tests. Serum electrolytes, total protein, and glucose were within the normal range, and both groups concentrated urine when deprived of water. Levels of all omega-3 fatty acids in red blood cells were greatly depressed in POST monkeys, while levels of omega-6 fatty acids were elevated or unchanged. These results confirm the effects of PRE+POST deficiency on fluid intake and demonstrate that postnatal deficiency by itself is sufficient for the effects.

Absorption of the n-3 eicosapentaenoic and docosahexaenoic acids as ethyl esters and triglycerides by humans.

Five normolipemic subjects received three test meals containing 28 g n-3 (omega-3) fatty acids provided as 1) triglycerides, 2) ethyl esters, and 3) ethyl esters + 12 g olive oil. The control meal contained olive oil. When equivalent amounts of fat were given, the increase in chylomicron and plasma triglycerides was similar; n-3 fatty acid contents were also similar after n-3 fatty acid intake as ethyl esters or triglycerides. Ethyl esters alone were well absorbed and produced similar n-3 fatty acid responses in plasma triglycerides and chylomicrons. At 24 h after the n-3 fatty acid-containing meals, the fatty acid plasma concentration of these acids was similar. This study showed that n-3 fatty acids in fish oil given as ethyl esters or triglycerides were equally well absorbed. Eicosapentaenoic and docosahexaenoic acids were also equally absorbed.

Biochemical and functional effects of prenatal and postnatal omega 3 fatty acid deficiency on retina and brain in rhesus monkeys.

Docosahexaenoic acid [22:6 omega 3; 22:6-(4,7,10,13,16,19)] is the major polyunsaturated fatty acid in the photoreceptor membranes of the retina and in cerebral gray matter. It must be obtained either from the diet or by synthesis from other omega 3 fatty acids, chiefly alpha-linolenic acid (18:3 omega 3). We tested the effect of dietary omega 3 fatty acid deprivation during gestation and postnatal development upon the fatty acid composition of the retina and cerebral cortex and upon visual function. Rhesus monkeys (Macaca mulatta) were fed semipurified diets very low in 18:3 omega 3 throughout pregnancy, and their infants received a similar diet from birth. A control group of females and their infants received a semipurified diet supplying ample 18:3 omega 3. In near-term fetuses and newborn infants of the deficient group, the 22:6 omega 3 content of phosphatidylethanolamine was one-half of control values in the retina and one-fourth in cerebral cortex. By 22 months of age, the content of 22:6 omega 3 in these tissues approximately doubled in control monkeys, but it failed to increase in the deficient group. Low levels of 22:6 omega 3 in the deficient animals' tissues were accompanied by a compensatory increase in longer-chain omega 6 fatty acids, particularly 22:5 omega 6. Functionally, the deficient animals had subnormal visual acuity at 4-12 weeks of age and prolonged recovery time of the dark-adapted electroretinogram after a saturating flash. Abnormally low levels of 22:6 omega 3 may produce alterations in the biophysical properties of photoreceptor and neural membranes that may underlie these functional impairments. The results of this study suggest that dietary omega 3 fatty acids are retina and brain.

Dietary omega-3 fatty acid deficiency and visual loss in infant rhesus monkeys.

Linolenic acid (18:3 omega 3) is a dietary precursor of docosahexaenoic acid (22:6 omega 3), the major fatty acid in the photoreceptor membranes of the retina. We hypothesized that rhesus monkeys deprived of dietary omega-3 fatty acids during prenatal and postnatal development would show plasma depletion of these fatty acids and visual impairment. Semipurified diets low in omega-3 fatty acids were fed to one group of adult female rhesus monkeys throughout pregnancy and to their infants from birth. A control group of mothers and infants received similar diets but supplying ample linolenic acid. In the plasma phospholipids of deficient infants, linolenic acid was generally undetectable and 22:6 omega 3 levels became progressively depleted, falling from 42% of control values at birth to 21% at 4 wk, 9% at 8 wk, and 6% at 12 wk of age. In the other plasma lipid classes, 22:6 omega 3 was undetectable by 12 wk. The visual acuity of the deprived infants, as measured by the preferential looking method, was reduced by one-fourth at 4 wk (P less than 0.05) and by one-half at 8 and 12 wk (P less than 0.0005) compared with control infants. These results suggest that omega-3 fatty acids may be an essential nutrient, and that 22:6 omega 3 may have a specific function in the photoreceptor membranes of the retina.