Nutrition and the Heart

Ramalingaswami, V.

doi:10.1159/000166102

Cited by 14 publications

(3 citation statements)

References 6 publications

(7 reference statements)

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“…This conclusion is supported by case reports and small studies of patients on fasting diets that have reported sudden cardiac death and myofibrillar damage (Ahmed, Flynn, & Alpert, 2001). The chief finding was myocardial atrophy, which is consistent with protein calorie malnutrition in humans (Ramalingaswami, 1968;Schnitker, Mattman, & Bliss, 1951) and monkeys (Chauhan, Nayak, & Ramalingaswami, 1965). What is particularly worrisome is that myocardial atrophy of myocardial cells occurred after merely 2 weeks on a diet that provided 40% of normal caloric intake, which is at least twice as much kilocalories per day as in the above related studies (Chauhan et al, 1965;Ramalingaswami, 1968;Schnitker et al, 1951).…”

Section: Discussionmentioning

confidence: 52%

Short‐term very low caloric intake causes endothelial dysfunction and increased susceptibility to cardiac arrhythmias and pathology in male rats

Almeida

Shults

Souza

et al. 2020

Experimental Physiology

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New Findings What is the central question of this study? What are the effects of a 2 week period of severe food restriction on vascular reactivity of resistance arteries and on cardiac structure and function? What is the main finding and its importance? This study showed, for the first time, that a 2 week period of severe food restriction in adult male Fischer rats caused endothelial dysfunction in mesenteric arteries and increased the susceptibility to ischaemia–reperfusion‐induced arrhythmias and cardiac pathology. Our findings might have ramifications for cardiovascular risk in people who experience periods of inadequate caloric intake. Abstract Severe food restriction (sFR) is a common dieting strategy for rapid weight loss. Male Fischer rats were maintained on a control (CT) or sFR (40% of CT food intake) diet for 14 days to mimic low‐calorie crash diets. The sFR diet reduced body weight by 16%. Haematocrits were elevated by 10% in the sFR rats, which was consistent with the reduced plasma volume. Mesenteric arteries from sFR rats had increased sensitivity to vasoconstrictors, including angiotensin II [maximum (%): CT, 1.30 ± 0.46 versus sFR, 11.5 ± 1.6; P < 0.0001; n = 7] and phenylephrine [maximum (%): CT, 78.5 ± 2.8 versus sFR, 94.5 ± 1.7; P < 0.001; n = 7] and reduced sensitivity to the vasodilator acetylcholine [EC 50 (n m ): CT, 49.2 ± 5.2 versus sFR, 71.6 ± 6.8; P < 0.05; n = 7]. Isolated hearts from sFR rats had a 1.7‐fold increase in the rate of cardiac arrhythmias in response to ischaemia–reperfusion and more cardiac pathology, including myofibrillar disarray with contractions and cardiomyocyte lysis, than hearts from CT rats. The sFR dietary regimen is similar to very low‐calorie commercial and self‐help weight‐loss programmes, which provide ∼800–1000 kcal day −1 . Therefore, these findings in rats warrant the study of cardiovascular function in individuals who engage in extreme dieting or are subjected to bouts of very low caloric intake for other reasons, such as socioeconomic factors and natural disasters.

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Section: Discussionmentioning

confidence: 52%

Short‐term very low caloric intake causes endothelial dysfunction and increased susceptibility to cardiac arrhythmias and pathology in male rats

Almeida

Shults

Souza

et al. 2020

Experimental Physiology

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“…This conclusion is supported by case reports and small studies of patients on fasting diets that have reported sudden cardiac death and myofibrillar damage [ 28 ]. The chief finding was myocardial atrophy, which is consistent with protein calorie malnutrition in humans [ 29 , 30 ] and monkeys [ 31 ]. What is of particular concern is the lasting cardiac damage in female rats that is evident 3 months after BW has returned to CT levels.…”

Section: Discussionmentioning

confidence: 53%

Susceptibility of female rats to cardiac arrhythmias following refeeding after severe food restriction

et al. 2022

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Background Many studies have shown malnutrition and inadequate caloric consumption have adverse acute effects on cardiovascular structure and function. Methods To determine the adverse long term cardiovascular effects, we studied cardiac morphology and function in female (F) and male (M) severe food restricted rats 3 months after refeeding (sFR-Refed). Results Two weeks of a normal chow diet in which calories were reduced by 60% decreased body weight (BW) by approximately 15% in both sexes. Within 2 weeks of refeeding, no differences in BW were detected between CT and sFR-Refed groups. However, male rats gained almost 3 times more BW than the females over the 3-month refeeding period. Sex differences were also observed in cardiac pathology. Hearts from F-sFR-Refed rats exhibited more atrophy and less hypertrophy, while M-sFR-Refed rats predominantly exhibited hypertrophic remodeling. While there were no differences in the frequency of ventricular arrhythmias induced by ischemia/reperfusion (I/R) in the isolated heart between M-CT and M-sFR-Refed rats, I/R induced twice as many arrhythmias in the F-sFR-Refed rats compared to F-CT. Conclusions These findings indicate the female heart is more susceptible to the long term adverse cardiovascular effects of sFR months after refeeding. Thus, this study provides a rationale for studying sex differences in cardiovascular risk in individuals who experience sFR for voluntary (e.g., very low-calorie dieting) or involuntary (e.g., poverty) reasons earlier in life.

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“…Significant functional, metabolic, and morphological changes take place in the heart in states of protein and caloric malnutrition (Sirnonson et aI., 1948;Gopalan et al, 1955;Srnythe et aL, 1962;Chauhan et al, 1965;Rarnalingaswarni, 1968;Gopalan and Srikantia, 1973;McKinney, 1974;Abel et al, 1979;Rossi et al, 1980). Since (a) the catecholamines have important inotropic and metabolic effects on the heart (Opie, 1969;Mayer, 1974;Braunwald et aI., 1976), (b) the catecholamines are myocardial hypertrophy-inducing agents (Laks et al, 1973), but they can also be destructive to the myocardium (Raab, 1953(Raab, , 1963Rona et al, 1959;Ferrans et al, 1969), (c) the catecholamines are synthesized from tyrosine and/or phenylalanine, and the ultimate source of both these amino acids is dietary protein, and (d) several prior studies have disclosed alterations in noradrenaline and adrenaline metabolism in protein-calorie malnutrition (Shoemaker and Wurtrnan, 1970;Hoeldtke and Wurtrnan, 1973;Edozien et al, 1975;Stern e t al., 1975), the current investigation has been undertaken to study the catecholamine levels in the hearts of rats subjected to protein-calorie malnutrition and a~er a period of nutritional rehabilitation.…”

Section: Introductionmentioning

confidence: 99%

Effect of protein-calorie malnutrition on catecholamine levels and weight of heart in rats

Rossi

Oliveira

Zucoloto

et al. 1980

J. Neural Transmission

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Catecholamine levels and weight of heart were studied in rats subjected to protein-calorie malnutrition and after a period of nutritional rehabilitation. Rats given a protein deficient diet (4% protein) for periods of 6 and 12 weeks showed a severe restriction of body weight gain. Nevertheless, even though the measured heart weight of deficient rats was significantly lower than the respective controls (16% protein), the deficient rats incurred "real" cardiac enlargement since the mean heart weight of the equal body weight controls was significantly different from that of the deficient animals. The mean heart weight of rats fed a high-protein diet for 6 weeks thereupon a 6-week period of protein deprivation was still less than that of controls, and the heart ratio was still greater than that of controls. However, the heart weight of rehabilitated rats was not significantly different from that of equal body weight controls. Serum protein and albumin levels in dificient rats were significantly decreased in comparison to rats fed a high-protein diet. While the serum protein levels of rehabilitated rats were lower than those of controls, the albumin levels were not different. The protein-calorie malnourished rats, which received a low-protein diet for 6 and 12 weeks, showed a significant increase in myocardium noradrenaline concentration. After a period of nutritional rehabilitation this change did not persist. These catecholaminergic alterations in heart may be responsible, at least in part, for the different cardiac abnormalities described as a result of protein-calorie dietary deficiency. It may also explain the "real" cardiac enlargement observed in deficient rats, according to the hypothesis that noradrenaline may be the ultimate myocardial hypertrophy hormone.

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Nutrition and the Heart

Cited by 14 publications

References 6 publications

Short‐term very low caloric intake causes endothelial dysfunction and increased susceptibility to cardiac arrhythmias and pathology in male rats

Short‐term very low caloric intake causes endothelial dysfunction and increased susceptibility to cardiac arrhythmias and pathology in male rats

Susceptibility of female rats to cardiac arrhythmias following refeeding after severe food restriction

Effect of protein-calorie malnutrition on catecholamine levels and weight of heart in rats

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