Posted by desolationrower on March 30, 2011, at 20:58:16
In reply to has anyone done ketogenic diet + antidepressants, posted by desolationrower on March 25, 2011, at 6:15:13
The other thing i was thinking about was just related to cortisol - (study 1): ketosis had greater cortisol, for overweight..
and this (cortisol stuff) is probably less relevent if you are in perfect health.
Trying to remember hpa & sympathetic system interaction with antidepressants plus with glucose system just makes my head hurt. I need one of those full-wall diagrams.
while sris improved things, nris made the typical problems worse, and MAOIs caused hypoglycemia (more of a rebound situation) (see study 2, note that i think this might also have to do with 5ht2 receptors). Which is what i was first thinking about: could MAOI afternoon drowsiness be hypoglycemia related? weight gain seems worse with phenelzine, and there is some evidence the hypoglycemia is related to the structure, instead of/in addition to MAOI effect.
anyway, i guess my main point is that if you are a bit insulin resistant, this might affect AD choice. and maybe has something to do with the melancholic/atypical thing, which might point toward some particular dietary options depending on the type of depression. This study found a difference: worse glucose disposal for atypical, and worse c-peptide.[3] from the abstract i'm not sure they restricted it to unmedicated people tho.
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STUDY 1:
Dietary macronutrient content alters cortisol metabolism independently of body weight changes in obese men.Abstract
CONTEXT: Dietary macronutrient composition influences cardiometabolic health independently of obesity. Both dietary fat and insulin alter glucocorticoid metabolism in rodents and, acutely, in humans. However, whether longer-term differences in dietary macronutrients affect cortisol metabolism in humans and contribute to the tissue-specific dysregulation of cortisol metabolism in obesity is unknown.
OBJECTIVE: The objective of the study was to test the effects of dietary macronutrients on cortisol metabolism in obese men.
DESIGN: The study consisted of two randomized, crossover studies.
SETTING: The study was conducted at a human nutrition unit.
PARTICIPANTS: Participants included healthy obese men. INTERVENTIONS, OUTCOME MEASURES, AND RESULTS: Seventeen obese men received 4 wk ad libitum high fat-low carbohydrate (HF-LC) (66% fat, 4% carbohydrate) vs. moderate fat-moderate carbohydrate (MF-MC) diets (35% fat, 35% carbohydrate). Six obese men participated in a similar study with isocaloric feeding. Both HF-LC and MF-MC diets induced weight loss. During 9,11,12,12-[(2)H](4)-cortisol infusion, HF-LC but not MF-MC increased 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) activity (rates of appearance of cortisol and 9,12,12-[(2)H](3)-cortisol) and reduced urinary excretion of 5alpha- and 5beta-reduced [(2)H](4)-cortisol metabolites and [(2)H](4)-cortisol clearance. HF-LC also reduced 24-h urinary 5alpha- and 5beta-reduced endogenous cortisol metabolites but did not alter plasma cortisol or diurnal salivary cortisol rhythm. In sc abdominal adipose tissue, 11beta-HSD1 mRNA and activity were unaffected by diet.
CONCLUSIONS: A low-carbohydrate diet alters cortisol metabolism independently of weight loss. In obese men, this enhances cortisol regeneration by 11beta-HSD1 and reduces cortisol inactivation by A-ring reductases in liver without affecting sc adipose 11beta-HSD1. Alterations in cortisol metabolism may be a consequence of macronutrient dietary content and may mediate effects of diet on metabolic health.
STUDY 2
The effect of antidepressants on glucose homeostasis and insulin sensitivity: synthesis and mechanisms
2006
Objective: To synthesise results from investigations reporting on the effect of antidepressants on glucoseinsulin homeostasis. Method: The authors conducted a MedLine search of all English language articles from 1966 to October 2005 using the keywords: bipolar disorder, major depressive disorder, diabetes mellitus, glucose homeostasis, and the name of each antidepressant that has been indicated for major depression in Canada and the US up to October 2005. The search was supplemented with a manual review of relevant references. Both preclinical and clinical investigations were reviewed. Results: Some serotonergic antidepressants (e.g., fluoxetine) reduce hyperglycaemia, normalise glucose homeostasis and increase insulin sensitivity, whereas some noradrenergic antidepressants (e.g., desipramine) exert opposite effects. Dual-mechanism antidepressants (e.g., duloxetine and venlafaxine) do not appear to disrupt glucose homeostatic dynamics, whereas nonselective hydrazine monoamine oxidase inhibitors (e.g., phenelzine) are associated with hypoglycaemia and an increased glucose disposal rate. Conclusion: Some antidepressants exert a clinically significant effect on metabolism relevant to both therapeutic outcome and adverse events.STUDY 3
Disturbed Glucose Disposal in Patients With Major Depression; Application of the Glucose Clamp TechniqueObjective: To assess the whole-body glucose disposal in patients with both typical and atypical depression and to characterize the neuroendocrine responses during a hyper-, eu-, hypoglycemic stepwise clamp experiment in patients with both subtypes of major depression. Depressive disorders and alterations in glucose metabolism are closely associated. The glucose clamp technique is considered to be the "gold standard" for the assessment of whole-body glucose disposal.
Methods: We studied 19 patients with typical major depressive disorder (MDD), 7 patients with atypical major depression, and 30 men and women of a healthy comparator group using a stepwise glucose clamp procedure. Glucose disposal rates were assessed and concentrations of hormones involved in glucose allocation were measured.
Results: Glucose disposal rates were lower by 19% in patients with typical MDD and 30% in patients with atypical MDD than in the group of healthy controls (3.2 ± 0.8 and 2.8 ± 0.7 versus 4.0 ± 1.0 mmol h1 kg1). C-peptide concentrations were 26% higher in patients with atypical MDD and similar in patients with typical MDD and healthy controls. Vascular endothelial growth factor concentrations were 30% higher in typical MDD and similar in atypical MDD and the control group.
Conclusions: Whole-body glucose disposal is reduced in patients with typical and atypical depression. The observed neuroendocrine responses suggest a hyperactive allocation system in typical depression and a hypoactive allocation system in atypical depression.
-d/r
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thread:981091
URL: http://www.dr-bob.org/babble/20110321/msgs/981503.html