I took olanzapine 2 and a half years ago and have since then acquired various medical problems.
After being traumatized one too many times without apologies I just couldn’t bounce back the same nor forgive as easily anymore after thinking I was stable again in a safe emvironment.
I get tired of the cycle of weight loss after medication so I’m like this weight loss expert but have no control over my body again when on meds, especially after Zyprexa. Zyprexa seemed to work for my mood, but I felt like sleeping too much and my legs felt irritable and I had perpanerol for that, but I felt weak all the time and dizzy and like I couldn’t even hold my niece for long. I gained 6 pounds a week. I tried preparing for it this time because of the previous times of my weight went up on medication and I’d blame myself and then up went my cholesterol and then back down after meds after hard work. I tried working out twice a day and although I did feel hungry I avoided food, but Nooo it was the worst weight gain by far and I could feel my skin stretching and it didn’t feel like a normal healthy weight gain either and before at least retained I a shape and a waist, but thus just came on with higher fat proportions and maybe visceral fat who knows? My perfect labs started to get effected after my years of eating healthy trying to avoid the diabetes in my family and from my little skinny grandma. Did I say on this genetic site that they keep updating I have a varying health score of A+ for weight, D-F for schizophrenia, A+ for personality (I guess bc of empathy that gets effected with hardship) and a downgraded F for diabetes and better score for cholesterol levels. It gave me an A for depression… haha and A+ for possible weight gain hahaha, but did lists medications and said I’d most likely gain weight on Zyprexa. Well now since getting schizophrenia I’ve gotten depressed and apathetic some days and the weight… . It does say I do well on Zyprexa, but there’s more risk of weight gain. My sugar cholesterol had been better before, sugar was low and now… changing. I recommend getting your dna done at ancestry or my heritage then putting it on SelfDecode for $50 a year for their research site and ever changing health report based on you’re dna although not perfect and environment matters a lot too, but it explains some things. I moved and at the er asked about my metabolism and it was a relief to hear that weight loss is very hard and it’s wasnt so much my fault. They told me the truth and said it was notorious for weight gain. They would not fix it but it was kind of a slap in the face to be offered nutritious advice classes or portion control by those who never took this when weight was manaeageble before meds and healthy eating.
I learned also that Zyprexa may affect B12 metabolism and cause deficiency when I suddenly started getting shocks to the right side of my face recently where I was hit by a truck six years ago and it spread to the whole right side and gets more intense with swallowing or air or being awake… or the weather so my dr said maybe B12 or folic acid (B9) which go hand in hand. The next dr she referred me to said my B12 level was 3,000 almost and fine but to me that was off the charts and I don’t know if it was the gel test and not metabolized and it does okay a role in helping to turn fat into energy to use so I asked for a retest and folic acid test to name sure it’s not a deficiency or metabolism problem with B12 or folic acid. How do you fix that? My TSH is 1.89 out of 5, which is good but it’s one of many metabolisms. I read some online stories that B12 metabolism is a common issue with patients on olanzapine. They said it’d take time to get out of my system and I’m grateful for my stomach finally growling but I’m so tired and exercising is not as enjoyable or easy and humiliating and less able at this weight. Doing things are so different and harder now and I wear out easier and I feel pity for all with these problems bc you basically suffer 24/7 if you’re expected to live like this with the excess. Schizophrenia is hard but… sigh. So much judgement and ppl assuming you’re lazy and it’s lack of education in nutrition. I made an A+… and still don’t get it and please… females are programmed to get obsessed with being thin and eating disorders so… why assume it’s portion control? Anyway… I read a study I’ll post how some ppl say you could gain weight up to two years after stopping Zyprexa and another study that is studying short term meds to try to lessen the fat increase. There is also I study I’d like to post below about how Zyprexa starts to use fat for energy instead of the usual carbs which sounds good, but not so much because then it starts lessening your muscle and increasing fat in new areas and your fat percentage changes, but the articles do a fat better job. I’m hoping that my body goes back to metabolizing the way it used to and gaining muscle instead of more fat. I read a scary article that you can keep gaining weight up to two years after stopping Zyprexa but there is a study below on meds they’re trying with Zyprexa to prevent weight gain.
https://thelastpsychiatrist.com/2010/10/zyprexa_and_fat.html
The Last Psychiatrist
Wovon man nicht sprechen kann, darüber muß man schweigen.
OCTOBER 18, 2010
Why Zyprexa (And Other Atypical Antipsychotics) Make You Fat
annalynne_mccord_90210.jpg
this post does not apply to her, she only eats apples
Strange finding: Zyprexa makes free fatty acids level go down.
Wait, isn’t that a good thing?
II. Zyprexa’s effects on glucose and insulin are bad.
In a rat study of rats, using rats, Zyprexa raised glucose levels by 20%, both in fed and fasting states.
It didn’t much increase insulin in fed states (already high) but it kept insulin high even in fasting states: at 14h post meal, it was 140% higher than it should have been. All that exposure to insulin, for so long. At the coffee cart, we doctors would call that bad.
III. Zyprexa’s effect on triglycerides is… weird.
Zyprexa made circulating triglyceride levels fall-- it promoted the uptake of free fatty acids by various tissues:
zyprexa triglycerides.png
All those tissues taking up fatty acids-- what did they do with it?
IV. Zyprexa Makes Your Body Use Fat, Not Carbs, As Fuel
Normally, after eating, your body uses carbohydrate as the main energy source. After a long time hungry, it switches to fat.
Zyprexa made the body use fat all the time:
zyprexa rer.png
RER (respiratory exchange ratio) tells you what’s being used: 1= carbs, 0.85= carb/fat mix, and .7 is all fat. You eat, and your body uses carbs. After a few hours, your body switches to fat utilization.
In graph A, in the first 3 hours the body should have been using carbs and fat; but with Zyprexa, it was preferring mostly fat.
In graph B, every time you got a Zyprexa dose, your body switched to fat utilization instead of carbs.
V. Wait a second, why would increased utilization of fat be a bad thing?
If the body is churning through the fat, what do you think it is doing with all the sugar? Answer: turning your arteries into Twizzlers. Yum!
The typical thinking is that hyperglycemia leads to insulin resistance leads to increased fatty acid utilization. But that might be the wrong direction: it seems that the increased fatty acid utilization means sugar is unused (hyperglycemia) and remains high well into the fasting state, with consequent high levels of insulin. Insulin high too long becomes tolerance to insulin becomes insulin resistance becomes BKA.
VI. SUMMARY: A class effect, to varying degrees; and eating less may not help.
-
Food intake was the same between controls and Zyprexaers. You get these effects even if you eat the same.
-
This effect is shared by other atypicals, in a predictable fashion:
atypicals rer fed.pngIn the fed state, Zyprexa and Clozaril do a massive conversion to fat utilization, Risperdal a medium, and sulpiride minimal covnersion.
In the fasting state:
atypical rer fasting.pngGeodon has a lesser effect than Zyprexa, and appears to normalize; Abilify and Haldol seem close to normal.
-
These effects are consistent with Lilly’s own studies that the majority of weight gain happens in the first month, and not suddenly after a year of use.
-
There is still a hunger component to weight gain that is separate from the metabolic effect. Some drugs will make you hungry, change your metabolism, or some mixture of the two. Hunger appears to be a H1 mediated process (Seroquel, Zyprexa, Clozaril, Remeron, Paxil>Prozac, etc.)
-
The immediate clinical consequence of this information is probably (paradoxically) to tell the patients to eat less sugar.
Unless you dramatically cut fat out of your diet, the body will still churn through what fat you do eat at the expense of carbohydrate. Better, and easier, to reduce the carb load that lingers in your body (and likely ultimately gets stored.)
VII. Is that all the bad news?
No, of course not!
In another study (same authors, same topic, same time-- two completely different journals; thanks promotions committee, turning academics into bloggers one study at a time) they found that while there was increased lipogenesis (storage), the rats didn’t have a change in body weight.
In other words, Zyprexa didn’t make them heavier, it made them fatter. It increased their body fat while decreasing the lean body mass. Bright side: now they can float!
Add to this that it though caloric intake was the same, it dramatically decreased locomotor activity. So same calories, but less calorie need.
VIII. Well thank God doctors are finally going to know the truth about Zyprexa!
From who(m)?
The reality is I found these two articles by accident, researching a blog post about something else entirely. I would never have found this article, let alone the other article, on my own. And I read a lot.
Ordinarily, this kind of information would have come to me through my Abilify rep: “see? Zyprexa blows!” But the FDA now forbids anti-competitor comparisons; and neither are the reps allowed to tell me that the study exists. Promotional speakers can’t mention this either. So? CME? BWAHAHAHAHAHAHAHAHA!
Here’s the bottom line, and it applies to all speech everywhere: either you permit all kinds of speech, and let the truth battle on its merits; or you permit only one line of speech-- and let the truth, if it was suppressed, come up like smoke through cracks. But when you permit some speech and block others-- when you create gatekeepers of speech-- it creates the impression that the truth is in the permitted speech. Most of the time, it’s not.
PubMed Central (PMC)
Protection from olanzapine-induced metabolic toxicity in mice by acetaminophen…
In mice and in humans, treatment with the second generation antipsychotic drug olanzapine (OLZ) produces excessive weight gain, adiposity and secondary metabolic complications, including loss of glucose and insulin homeostasis. In mice consuming a…
Abstract
Objective
In mice and in humans, treatment with the second generation antipsychotic drug olanzapine (OLZ) produces excessive weight gain, adiposity and secondary metabolic complications, including loss of glucose and insulin homeostasis. In mice consuming a high fat (HF) diet, a similar phenotype develops, which is inhibited by the analgesic acetaminophen (APAP) and by the antioxidant tetrahydroindenoindole (THII). Therefore, we examined the ability of APAP and THII to prevent metabolic changes in mice receiving OLZ.
Design and Measurement
C57BL/6J mice received either a normal diet or a high fat diet, and were administered OLZ (3 mg/kg body weight/d), alone or with APAP (35 mg/kg body weight/d) or THII (4.5 mg/kg body weight), for 10 weeks. Parameters of body composition and metabolism, including glucose and insulin homeostasis and oxidative stress, were examined.
Results
OLZ treatment doubled the HF diet-induced increases in body weight and percent body fat. These increases were partially prevented by both APAP and THII, although food consumption was constant in all groups. The THII protection was associated with an increase in whole body and mitochondrial respiration. OLZ also exacerbated, and both APAP and THII prevented, HF diet-induced loss of glucose tolerance and insulin resistance. Since increased body fat promotes insulin resistance by a pathway involving oxidative stress, we evaluated production of reactive oxygen and lipid peroxidation in white adipose tissue (WAT). HF diet caused an increase in lipid peroxidation, NADPH-dependent O2 uptake and H2O2 production, which were further exacerbated by OLZ. APAP, THII, and the NADPH oxidase inhibitor, diphenyleneiodonium chloride (DPI) each abolished oxidative stress in WAT.
Conclusions
We conclude that both APAP and THII intervene in the development of obesity and metabolic complications associated with OLZ treatment.
Keywords: Acetaminophen, Diet, Mice, Obesity, Olanzapine, Oxidative stress
Go to:
Introduction
Obesity poses a growing global health threat, due in large part to the consumption of diets high in fat content, coupled with sedentary lifestyles (1). Another risk factor for gain in body weight and adiposity are the use of drugs for treatment of psychotic disorders. These atypical (second-generation) antipsychotic drugs, such as olanzapine (OLZ; Zyprexa™; 2-methyl-4-(4-methyl-1-piperazinyl)-10H-thieno[2,3-b][1,5]-benzodiazepine) are used to treat millions of people suffering from psychotic episodes. While highly effective for their intended use, a high percentage of patients exhibit unfortunate secondary complications associated with the excess weight and obesity, including cardiovascular disease, dyslipidemia, and the development of insulin resistance and type 2 diabetes mellitus (T2DM), cardiovascular disease and stroke (2–4). It is therefore not surprising that a recent study found that persons with schizophrenia lose about 25 years of potential life due to premature cardiovascular mortality (5).
Standard anti-diabetic drugs such as metformin and thiazolidinediones (e.g., rosiglitazone, piaglitazone), or off-label drugs such as the anti-epileptic topiramate (Topamax™), are often prescribed with OLZ to prevent the development of metabolic complications, especially hyperglycemia (6). However, these prescription medications are expensive and have their own adverse side effects that tend to limit their use.
Mice are similar to humans by increasing body weight and adiposity when consuming a high fat diet (HF diet), and thus mouse models have proven useful for the study of metabolic disorders associated with a HF diet (7;8). In mice, acetaminophen (APAP; 20 mg/kg body weight/day) ameliorated the HF diet-induced gain in body weight and fat mass, and the associated metabolic complications (9;10). Histological examination of tissues that exhibit toxicity with high-dose APAP treatment (liver, kidney, olfactory epithelium) showed no evidence of toxicity under our dosing regimen (9). Similar to APAP, tetrahydroindenoindole (THII; 4b,5,9b,10-tetrahydroindeno[1,2-b]indole), prevented metabolic complications associated with excess weight and obesity that result from a HF diet (11). Therefore, we evaluated the potential for APAP and THII to protect against metabolic toxicity induced by OLZ in mice. APAP and/or THII may offer inexpensive alternatives or adjuvant therapy with drugs commonly used to treat metabolic disorders.
Go to:
2. Materials and Methods
2.1. Chemicals
OLZ was obtained from Thermo Fisher Scientific (Pittsburgh, PA). THII was synthesized as described and was 98% pure as determined by NMR and GC/MS (12). All other chemicals and reagents were from Sigma-Aldrich Chemical Company (St. Louis, MO) as the highest available grades.
2.2. Animals and treatment
https://www.drperlmutter.com/zyprexa-alters-metabolism/
How Zyprexa Alters Your Metabolism
Zyprexa, is an incredibly popular psychiatric medication manufactured by Eli Lilly. Yet, although Zyprexa was originally developed for the treatment of schizophrenia and bipolar disorder, it has now gained widespread use for the treatment of depression as well.
Back in 2007, Lilly was required to add a strong warning label to Zyprexa indicating the drugs tendency to cause weight gain, high blood pressure, and other metabolic problems. It was found that weight gain could continue for as long as two years after the medication was stopped and that one in six patients who took the medication would gain more than 33 pounds after two years of using it. And this is information that was added to the label.
These issues, weight gain and changes in metabolism, profoundly threaten long-term health. The relationship with respect to the drug is clear, but what hasn’t been well defined is the actual mechanism by which Zyprexa causes these events to occur.
A new study brings to our attention some very important new science as relates to this mechanism. The research, hearing in the journal, Translational Psychiatry, evaluated the effects of Zyprexa (generic name olanzapine) on the gut bacteria of laboratory animals. The animals received Zyprexa for 21 days given by injection into the abdominal cavity.
Dramatic changes were seen in the array of gut bacteria in animals who received Zyprexa and these changes were associated with significant weight gain, Inflammation, and fat deposition.
When the experimental animals also were given specific antibiotics that kept certain bacterial species from growing, these metabolic changes did not occur as aggressively when the Zyprexa was administered. The authors concluded:
These results suggest that the gut microbiome has a role in the cycle of metabolic dysfunction associated with olanzapine, and could represent a novel therapeutic target for preventing antipsychotic-induced metabolic disease.
I present this information to again drive home the point that so much of what occurs to change human metabolism in a dysfunctional way leading to things like diabetes, weight gain, autoimmunity, and inflammation, has its genesis in the gut bacteria. Changes in the gut bacteria can take place not only based upon our food choices, but as a consequence of various pharmaceutical drugs that are so commonly prescribed. This takes the notion of “above all do no harm” to a new level as, in moving forward, we need to consider how drugs alter the highly influential gut microbiome.