Similarities of Carbohydrate Deficiency and Fasting

Azar, Gordon J.

doi:10.1001/archinte.1963.03860030092007

Cited by 33 publications

(5 citation statements)

References 14 publications

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“…Since plasma free fatty acid levels may reflect both the rate of production of free fatty acids and determine their rate of uptake by the tissues (Armstrong et al, 1961) one might expect a relationship between plasma free fatty acids and ketonaemia. Several studies have failed to confirm this in vivo (Werk et al, 1961;Azar and Bloom, 1963;Genuth, 1966;Willms et al, 1969), though during a simple fast there appears to be an exponential relationship (Hanson et al, 1965). The present investigations (Table II, Figs.…”

Section: Discussioncontrasting

confidence: 49%

Ketonaemia in Uncontrolled Diabetes Mellitus

Watkins¹,

Hill²,

Fitzgerald³

et al. 1970

BMJ

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Section: Discussioncontrasting

confidence: 49%

Ketonaemia in Uncontrolled Diabetes Mellitus

Watkins¹,

Hill²,

Fitzgerald³

et al. 1970

BMJ

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“…As indicated in Figure 2, restriction of dietary CHOs would counteract this signalling cascade by normalizing glucose and insulin levels in subjects with metabolic syndrome, in this way acting similar to calorie restriction/fasting [61,62]. Indeed, it has been shown in healthy subjects that CHO restriction induces hormonal and metabolic adaptions very similar to fasting [63-66]. Dietary restriction is able to inhibit mTOR signalling through a second, energy-sensing pathway by stimulating phosphorylation of AMP-activated protein kinase (AMPK) [67].…”

Section: Tumor Cell Metabolism - It's All About Glucosementioning

confidence: 99%

Is there a role for carbohydrate restriction in the treatment and prevention of cancer?

2011

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Over the last years, evidence has accumulated suggesting that by systematically reducing the amount of dietary carbohydrates (CHOs) one could suppress, or at least delay, the emergence of cancer, and that proliferation of already existing tumor cells could be slowed down. This hypothesis is supported by the association between modern chronic diseases like the metabolic syndrome and the risk of developing or dying from cancer. CHOs or glucose, to which more complex carbohydrates are ultimately digested, can have direct and indirect effects on tumor cell proliferation: first, contrary to normal cells, most malignant cells depend on steady glucose availability in the blood for their energy and biomass generating demands and are not able to metabolize significant amounts of fatty acids or ketone bodies due to mitochondrial dysfunction. Second, high insulin and insulin-like growth factor (IGF)-1 levels resulting from chronic ingestion of CHO-rich Western diet meals, can directly promote tumor cell proliferation via the insulin/IGF1 signaling pathway. Third, ketone bodies that are elevated when insulin and blood glucose levels are low, have been found to negatively affect proliferation of different malignant cells in vitro or not to be usable by tumor cells for metabolic demands, and a multitude of mouse models have shown anti-tumorigenic properties of very low CHO ketogenic diets. In addition, many cancer patients exhibit an altered glucose metabolism characterized by insulin resistance and may profit from an increased protein and fat intake.In this review, we address the possible beneficial effects of low CHO diets on cancer prevention and treatment. Emphasis will be placed on the role of insulin and IGF1 signaling in tumorigenesis as well as altered dietary needs of cancer patients.

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“…Early studies on starvation (Azar and Bloom 1963;Bloom and Azar 1963;Cahill 1981;Consolazio et al 1968) demonstrated the link between CHO insufficiency and ketosis. Consolazio et al (1968) similarly noted that when in a daily energy deficit of 11.7 MJ (2 800 kcal) induced through fasting and exercise, ketosis could be avoided by ingesting 1.8 MJ (420 kcal, ~100 g) of CHO per day, an amount equal to the carbohydrate requirements of the brain (Cahill 1981).…”

Section: Introductionmentioning

confidence: 99%

Carbohydrate intake and ketosis in self-sufficient multi-stage ultramarathon runners

Edwards

Elliott

Kitic

2019

Journal of Sports Sciences

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Ultra-endurance athletes accumulate an energy deficit throughout their events and those competing in self-sufficient multi-stage races are particularly vulnerable due to load carriage considerations. Whilst urinary ketones have previously been noted in ultra-endurance exercise and attributed to insufficient carbohydrate (CHO) availability, not all studies have reported concomitant CHO intake. Our aim was to determine changes in blood glucose and βhydroxybutyrate concentrations over five days (240 km) of a self-sufficient multi-stage ultramarathon in combination with quantification of energy and macronutrient intakes, estimated energy expenditure and evaluation of energy balance. Thirteen runners (8 male, 5 female, mean age 40 ± 8 years) participated in the study. Glucose and β-hydroxybutyrate were measured every day immediately post-running, and food diaries completed daily. CHO intakes of 301 ± 106 g•day -1 (4.3 ± 1.8 g•kg -1 •day -1 ) were not sufficient to avoid ketosis (5-day mean βhydroxybutyrate: 1.1 ± 0.6 mmol.L -1 ). Furthermore, ketosis was not attenuated even when CHO intake was high (9 g•kg -1 •day -1 ). This suggests that competing in a state of ketosis may be 44 inevitable during multi-stage events where load reduction is prioritised over energy provisions.Attenuating negative impacts associated with such a metabolic shift in athletes unaccustomed to CHO and energy restriction requires further exploration.

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Similarities of Carbohydrate Deficiency and Fasting

Cited by 33 publications

References 14 publications

Ketonaemia in Uncontrolled Diabetes Mellitus

Ketonaemia in Uncontrolled Diabetes Mellitus

Is there a role for carbohydrate restriction in the treatment and prevention of cancer?

Carbohydrate intake and ketosis in self-sufficient multi-stage ultramarathon runners

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