[bigrosiegreenbaum]

My shrink is trying to convince me to take a med for my bi-polar but I've been resisting because so many of them mess with blood sugar. The one that supposedly doesn't - Depakote - DOES put on weight, which eventually will affect blood sugar.

Has anyone had any experience with a bi-polar med that hasn't had a bad effect on bg? Don't know if we have many bi-polars on the forum...

 

[phraedus]

I also am BiPolar:

Here is some of my research on lithium and depakote.

The effects of lithium on glucose transport and metabolism in skeletal muscle are strikingly similar to the persistent effects of exercise. These results support the possibility that lithium might be useful in the treatment of insulin resistance in patients with non-insulin-dependent diabetes mellitus.

Our results demonstrated the ability of lithium ions to completely restore insulin sensitivity to normal in diabetic rats. The insulin-mimetic activity of the cation seems to be highly specific for the glycogenic pathway in skeletal muscle.

GSK-3 inhibitors protect against ER stress induced
cellular dysfunction
Valproic (2-propylpentanoic) acid is a small branch-chain
fatty acid and a potent and widely prescribed drug that acts
both as an anti-convulsant in the treatment of epilepsy and
as a mood-stabilizer to control bipolar disorder (Bowden et
al. 1994; Penry and Dean 1989).

valproic acid is depakote

We have shown that lithium, a selective inhibitor of GSK-
3 (Stambolic et al. 1996), and a synthetic GSK-3 inhibitor
II, 3-(3-carboxy-4-chloroanilino)-4-(3-nitrophenyl) maleimide,
can block lipid accumulation from glucosamine treatment
(Fig. 5) (Kim et al. 2005). The ability of 3 structurally
unrelated GSK-3 inhibitors to attenuate ER stress-induced
lipid accumulation strongly suggests that GSK-3 regulates
the pathways activated by ER stress. We hypothesize that
conditions of chronic hyperglycaemia associated with diabetes
mellitus can accelerate the development of atherosclerosis
by a mechanism that involves glucosamine-induced ER
stress and activation of GSK-3. Thus, inhibitors of GSK-3
may attenuate the development of atherosclerosis. Given the
variety of cellular functions it regulates, the use of GSK-3 as
a potential target for intervention therapy requires precise
control since its influence is necessary for many physiological
functions.

We conclude that lithium treatment stimulates rat beta-cell replication and long-term insulin secretion in vitro. These direct effects of the ion on the beta-cell may contribute to the antidiabetic effect of lithium encountered in animal models and patients.

I am a new member and thought I would reply to this post I am not yet allowed to post links if you want to see the referenced material Rosie I will send them to you in a PM.

 

[phraedus]

Another reference to GSK-3 inhibition by depakote.

Despite its wide use, the
specific molecular mechanisms responsible for the clinical
efficacy of valproate are not known. Exposure to millimolar
concentrations of valproate can induce a variety of cellular
responses that may be responsible for its clinical efficacy
(MacDonald and Bergey 1979; Phiel et al. 2003; Wang et
al. 1999; Williams et al. 2002). We and others have shown
that valproate can directly inhibit GSK-3a and -3b (Chen et
al. 1999; Werstuck et al. 2004).

 

[Shanny]

Much of Phraedus' research is taken verbatim from Pubmed and/or other diabetes sites. I suppose this is because he cannot post links, but after this, Phraedus, cite your sources.

 

[bigrosiegreenbaum]

Another reference to GSK-3 inhibition by depakote.

Despite its wide use, the
specific molecular mechanisms responsible for the clinical
efficacy of valproate are not known. Exposure to millimolar
concentrations of valproate can induce a variety of cellular
responses that may be responsible for its clinical efficacy
(MacDonald and Bergey 1979; Phiel et al. 2003; Wang et
al. 1999; Williams et al. 2002). We and others have shown
that valproate can directly inhibit GSK-3a and -3b (Chen et
al. 1999; Werstuck et al. 2004).

Thank you for your help, Phraedus, I'm going to see my doctor Thursday and talk about meds then. I really don't like medication at all....

 

[foxl]

Rosie I have an online friend who battles both BP and D. And she opted to take meds that affect BP adversely, because she felt it was the only way to control her BP. She eats low carb, and appears to be managing life pretty well.

 

[phraedus]

Thank you for your help, Phraedus, I'm going to see my doctor Thursday and talk about meds then. I really don't like medication at all....

Yes here's the downside to lithium and depakote.

Lithium is quite hard on the kidneys you can develop a tubal lesion which requires transplant or your micoralbumin ratio elevates after years of use. Also diabete insipidous is quite common.

Depakote depletes the body of carnitine this is an essential element in the mitochondrial chain for the use of free fatty acids makes it difficult to enter ketosis and you gain weight quite easily.\

Also contradicting studies on the effects of lithium on glucose, still unable to post links.

Effect of lithium on plasma glucose, insulin and glucagon in normal and streptozotocin-diabetic rats: role of glucagon in the hyperglycaemic response.
Hermida OG, Fontela T, Ghiglione M, Uttenthal LO.
Source

Centro de Investigaciones Biológicas, C.S.I.C., Madrid, Spain.
Abstract

1. Lithium salts, used in the treatment of affective disorders, may have adverse effects on glucose tolerance in man, and suppress glucose-stimulated insulin secretion in rats. 2. To study the interaction of these effects with pre-existing diabetes mellitus, plasma glucose and insulin responses to lithium chloride were measured in male Wistar rats made diabetic with intraperitoneal streptozotocin, and in normal controls. 3. In both normal and diabetic anaesthetized rats, intravenous lithium (4 mEq kg-1) caused a rise in plasma glucose. In absolute terms, the rise was greater in diabetic (5.2 mmol l-1) than in normal rats (2.3 mmol l-1). 4. Plasma insulin concentrations were reduced by lithium in normal rats, but the low insulin concentrations measured in the diabetic rats were not significantly changed. 5. After intravenous glucose (0.5 g kg-1), lithium-treated diabetic rats showed a second rise in plasma glucose at 60-90 min without any insulin response, while normal rats showed typically reduced insulin responses and initial glucose disappearance rates. 6. Intravenous glucose reduced plasma glucagon concentrations to a greater extent in normal than in diabetic rats, but lithium induced an equal rise in plasma glucagon in both groups, with a time-course similar to that of the hyperglycaemic effect. 7. The hyperglycaemic action of lithium is greater in the hypoinsulinaemic diabetic rats and appears to involve a stimulation of glucagon secretion in both normal and diabetic animals.

 

[bigrosiegreenbaum]

Yes here's the downside to lithium and depakote.

Lithium is quite hard on the kidneys you can develop a tubal lesion which requires transplant or your micoralbumin ratio elevates after years of use. Also diabete insipidous is quite common.

Depakote depletes the body of carnitine this is an essential element in the mitochondrial chain for the use of free fatty acids makes it difficult to enter ketosis and you gain weight quite easily.\

Also contradicting studies on the effects of lithium on glucose, still unable to post links.

Effect of lithium on plasma glucose, insulin and glucagon in normal and streptozotocin-diabetic rats: role of glucagon in the hyperglycaemic response.
Hermida OG, Fontela T, Ghiglione M, Uttenthal LO.
Source

Centro de Investigaciones Biológicas, C.S.I.C., Madrid, Spain.
Abstract

1. Lithium salts, used in the treatment of affective disorders, may have adverse effects on glucose tolerance in man, and suppress glucose-stimulated insulin secretion in rats. 2. To study the interaction of these effects with pre-existing diabetes mellitus, plasma glucose and insulin responses to lithium chloride were measured in male Wistar rats made diabetic with intraperitoneal streptozotocin, and in normal controls. 3. In both normal and diabetic anaesthetized rats, intravenous lithium (4 mEq kg-1) caused a rise in plasma glucose. In absolute terms, the rise was greater in diabetic (5.2 mmol l-1) than in normal rats (2.3 mmol l-1). 4. Plasma insulin concentrations were reduced by lithium in normal rats, but the low insulin concentrations measured in the diabetic rats were not significantly changed. 5. After intravenous glucose (0.5 g kg-1), lithium-treated diabetic rats showed a second rise in plasma glucose at 60-90 min without any insulin response, while normal rats showed typically reduced insulin responses and initial glucose disappearance rates. 6. Intravenous glucose reduced plasma glucagon concentrations to a greater extent in normal than in diabetic rats, but lithium induced an equal rise in plasma glucagon in both groups, with a time-course similar to that of the hyperglycaemic effect. 7. The hyperglycaemic action of lithium is greater in the hypoinsulinaemic diabetic rats and appears to involve a stimulation of glucagon secretion in both normal and diabetic animals.

Thanks for all that info! I'm seeing my doctor tomorrow and I'm going to tell her I don't want to be on meds at all.

 

[Patdart]

I have an online friend who participated in a study and found that as long as she can stay in ketosis, she requires no meds for her BP. So, her diet is very low carb.

Good luck,

 

[bigrosiegreenbaum]

I have an online friend who participated in a study and found that as long as she can stay in ketosis, she requires no meds for her BP. So, her diet is very low carb.

Good luck,

I'm still not clear on what ketosis means. Is it a good thing?

 

[Patdart]

Yes, it is! I've used it to lose 50 lbs and test several times a week. I keep my BG is line with it. I eat less than 30 g. of carb a day now and drink a lot of water and generally test at 40 on the Ketostix. I keep my fat and protein as a large part of my diet with low carb veggies.

 

[foxl]

WOW! I want to share that with my friend ...

The other GAD, GAD-65, is implicated in Bipolar ... and there is cross-reactivity between them, as well. Odd interesting stuff -- but no evidence of actual correlation that I have ever read.

 

[phraedus]

Ketosis simply means the body is using fat as the energy source .

If you are in ketosis you can tell by testing your urine with ketosis strips I find exercising first thing in the morning brings you ketonic (ketosis state)

This is the problem with depakote for me it is fine for a normal individual but I find going ketonic quite difficult on depakote.