From this week’s JAMA, a meta analysis: psychosis is as much a somatic disorder as a psychiatric one. Kraepelin was describing these changes 100 years ago. These aurhos have summarized the epidemiological data for us: the quote is from the abstract.
For these papers, instead of linkrot, I am going to put the reference in.
16 case-control studies comprising 15 samples met inclusion criteria. The overall sample included 731 patients and 614 controls. Fasting plasma glucose levels (Hedges g?=?0.20; 95% CI, 0.02 to 0.38; P?=?.03), plasma glucose levels after an oral glucose tolerance test (Hedges g?=?0.61; 95% CI, 0.16 to 1.05; P?=?.007), fasting plasma insulin levels (Hedges g?=?0.41; 95% CI, 0.09 to 0.72; P?=?.01), and insulin resistance (homeostatic model assessment of insulin resistance) (Hedges g?=?0.35; 95% CI, 0.14 to 0.55; P?=?.001) were all significantly elevated in patients compared with controls. However, HbA1c levels (Hedges g?=??0.08; CI, ?0.34 to 0.18; P?=?.55) were not altered in patients compared with controls.
These findings show that glucose homeostasis is altered from illness onset in schizophrenia, indicating that patients are at increased risk of diabetes as a result. This finding has implications for the monitoring and treatment choice for patients with schizophrenia.
Pillinger T, Beck K, Gobjila C, Donocik JG, Jauhar S, Howes OD. Impaired Glucose Homeostasis in First-Episode SchizophreniaA Systematic Review and Meta-analysis. JAMA Psychiatry. Published online January 11, 2017. doi:10.1001/jamapsychiatry.2016.3803
It is quite hard to get a fasting glucose but on an inpatient, with psychosis, due to disorganization. The current practice in NZ is to monitor glycosylated Hemoglobin(HbA1c) but these changes are late. Ir ia worth noting that these patients were antipsychotic naive or had less than two weeks treatment, and that the effect size, though significant, is small.
There is some data (I have seen presented)- that indicates that any antipsychotic will increase insulin resistance — and if it does not, it does not work. (I will admit that I was at a conference hearing early reports, not reading papers at the time). There is also a risk that we may over state a correlation and see causation. From a practical point of view, we do not as yet have enough information to change practice: we need trials that show that complications o diabetes are minimized in first episode if glucose resistance is treated from day one. My reading of the data suggests, to date, this is not the case.
The Glucose homeostasis changes are Effect not Cause. They bring on secondary, and severe, issues, but they’re not the driving force.
The Human body has a descending level of defense points. The Glucose up-shift is most likely because the nervous system requires more energy. The fastest way to do this is to shift Glucose, which increases the pass-through rate over the Blood-Brain barrier.
For something to be causal I’d want to see a big effect size: at least 0.6. Ain’t here.
ummm … can you translate this for me? 🙂
In short: if you look at people with their first episode of psychosis they have a higher blood glucose and their insulin does not work as well. This is a small to moderate change.
What Looking glass says is that this is not the cause. I agree that it is driven by something else. What we agree on is that this affects the body as well as the brain.
thank you for explaining … that’s what i thought it all meant.
having seen this up close and personal with my daughter … and my ex, who was diabetic (unmanaged b/c he did not manage it and ultimately was his cause of death), i often wondered if/what the correlation was, if any – of course not talking about a first episode here but multiple over years. i would agree it’s not the cause, but i’ve wondered if it’s not a trigger. i’m not a scientist at all, but i totally agree that it is a full system thing. cause? idk – but i suspect there are multiple. how it begins or is triggered? idk, but i know it’s complex, and by the time it’s over it’s systemic.
Some secondary effects are far more destructive than the primary disorder. Classically, it’s not the disorder that kills you, it’s the infections you pick up because of the disorder that does.