Have you experienced iron depletion from Tirzepatide use?

Musmadar

Member
I started using Tirzepatide more than 1 month ago, already lost about 6kg/13pounds...

The problem I have is that I started to feel very dizzy during workouts, especially legs workout...the same symptoms like anemia...and it has nothing to do with glucose being too low (that was the first thing I checked)

I was wondering if you have experienced the same....
 
I also found this article:

Tirzepatide and Iron Deficiency: A Growing Concern

Tirzepatide, a promising medication in the treatment of type 2 diabetes, has garnered attention not only for its efficacy but also for its potential side effects. Among these, the development of iron deficiency has emerged as a notable concern. Understanding the mechanism behind this adverse event and its clinical implications is crucial for healthcare providers and patients alike.

Tirzepatide belongs to a class of drugs known as GLP-1 receptor agonists, which work by mimicking the action of the glucagon-like peptide-1 (GLP-1) hormone. These medications stimulate insulin secretion, suppress glucagon release, and slow gastric emptying, resulting in improved glycemic control. However, emerging evidence suggests that GLP-1 receptor agonists may also impact iron metabolism.

One proposed mechanism for tirzepatide-induced iron deficiency revolves around its effect on gastric acid secretion. GLP-1 receptor agonists have been associated with reduced gastric acid production, potentially leading to impaired iron absorption in the duodenum, where acidic conditions are essential for iron solubility and uptake. Consequently, chronic use of tirzepatide may contribute to decreased iron levels over time.

Furthermore, the weight loss often observed with tirzepatide therapy could exacerbate the risk of iron deficiency. Rapid weight loss can deplete iron stores, as iron is stored in adipose tissue and released during periods of caloric restriction. Thus, patients undergoing significant weight reduction while on tirzepatide may be particularly susceptible to developing iron deficiency.

The clinical implications of tirzepatide-induced iron deficiency are multifaceted. Iron deficiency can lead to a spectrum of symptoms ranging from fatigue and weakness to more severe manifestations such as anemia. In patients with diabetes, iron deficiency may exacerbate pre-existing symptoms of fatigue, impacting their quality of life and potentially hindering adherence to diabetes management strategies. Moreover, untreated iron deficiency anemia can have serious consequences, including impaired cognitive function and diminished exercise tolerance.

Management strategies for tirzepatide-induced iron deficiency should aim to address both the underlying cause and the associated symptoms. This may involve oral or intravenous iron supplementation, dietary modifications to enhance iron absorption, and ongoing monitoring to ensure adequate iron repletion without overshooting and causing iron overload.

Its potential to induce iron deficiency underscores the importance of vigilant monitoring and proactive intervention.

So I'm interested in your opinion on the matter.
 
I wonder if the low iron affects body temperature control? I stay freezing on the stuff but haven’t done bloodwork since starting it over a year ago. Off n on usage.
When iron levels decline below optimal thresholds, it can disrupt thermoregulatory mechanisms, leading to alterations in body temperature.
One of the primary functions of iron is its participation in the synthesis of hemoglobin, the protein responsible for transporting oxygen from the lungs to tissues throughout the body. Oxygen consumption is intricately linked to metabolic heat production, whereby cells utilize oxygen to generate energy through cellular respiration. Consequently, inadequate iron levels can impair oxygen transport, limiting cellular energy production and subsequently reducing metabolic heat generation.
Beyond its influence on heat generation, iron deficiency can also affect thermoregulation by impairing heat dissipation mechanisms. Sweat glands, crucial for dissipating excess heat during periods of elevated body temperature, rely on adequate iron levels for optimal function. Iron deficiency can compromise sweat gland activity, diminishing the body's ability to dissipate heat efficiently. Consequently, individuals with low iron levels may experience difficulties in regulating body temperature, particularly during physical exertion or exposure to high ambient temperatures.

Furthermore, iron deficiency can disrupt thyroid function, exacerbating thermoregulatory dysfunction. Iron is essential for the synthesis of thyroid hormones, which play a central role in regulating metabolism and body temperature. Insufficient iron availability can impair thyroid hormone synthesis and function, leading to hypothyroidism characterized by a slowed metabolic rate and cold intolerance.

The consequences of impaired thermoregulation due to low iron levels extend beyond discomfort, potentially culminating in serious health complications. Prolonged exposure to suboptimal body temperatures can compromise immune function, increase susceptibility to infections, and exacerbate pre-existing health conditions. Additionally, individuals with iron deficiency may experience exacerbated symptoms of fatigue, lethargy, and cognitive impairment, further impeding their ability to cope with temperature fluctuations.
 
While tirzepatide primarily targets glucose and weight regulation through its actions on the incretin system, some studies have suggested potential associations between glucagon-like peptide-1 (GLP-1) receptor agonists—such as tirzepatide—and alterations in iron metabolism. Specifically, GLP-1 receptor agonists have been implicated in the regulation of hepcidin, a key hormone involved in iron homeostasis. Hepcidin modulates iron absorption in the intestines and its release from storage sites, and dysregulation of hepcidin levels can lead to disturbances in iron metabolism.
 
I also found this article:

Tirzepatide and Iron Deficiency: A Growing Concern

Tirzepatide, a promising medication in the treatment of type 2 diabetes, has garnered attention not only for its efficacy but also for its potential side effects. Among these, the development of iron deficiency has emerged as a notable concern. Understanding the mechanism behind this adverse event and its clinical implications is crucial for healthcare providers and patients alike.

Tirzepatide belongs to a class of drugs known as GLP-1 receptor agonists, which work by mimicking the action of the glucagon-like peptide-1 (GLP-1) hormone. These medications stimulate insulin secretion, suppress glucagon release, and slow gastric emptying, resulting in improved glycemic control. However, emerging evidence suggests that GLP-1 receptor agonists may also impact iron metabolism.

One proposed mechanism for tirzepatide-induced iron deficiency revolves around its effect on gastric acid secretion. GLP-1 receptor agonists have been associated with reduced gastric acid production, potentially leading to impaired iron absorption in the duodenum, where acidic conditions are essential for iron solubility and uptake. Consequently, chronic use of tirzepatide may contribute to decreased iron levels over time.

Furthermore, the weight loss often observed with tirzepatide therapy could exacerbate the risk of iron deficiency. Rapid weight loss can deplete iron stores, as iron is stored in adipose tissue and released during periods of caloric restriction. Thus, patients undergoing significant weight reduction while on tirzepatide may be particularly susceptible to developing iron deficiency.

The clinical implications of tirzepatide-induced iron deficiency are multifaceted. Iron deficiency can lead to a spectrum of symptoms ranging from fatigue and weakness to more severe manifestations such as anemia. In patients with diabetes, iron deficiency may exacerbate pre-existing symptoms of fatigue, impacting their quality of life and potentially hindering adherence to diabetes management strategies. Moreover, untreated iron deficiency anemia can have serious consequences, including impaired cognitive function and diminished exercise tolerance.

Management strategies for tirzepatide-induced iron deficiency should aim to address both the underlying cause and the associated symptoms. This may involve oral or intravenous iron supplementation, dietary modifications to enhance iron absorption, and ongoing monitoring to ensure adequate iron repletion without overshooting and causing iron overload.

Its potential to induce iron deficiency underscores the importance of vigilant monitoring and proactive intervention.

So I'm interested in your opinion on the matter.
If that is the case it is actually helpful for me. I have hemochromatosis which causes iron overload and must get blood drained every few months. Interesting though I had not seen this anywhere as a tirz side effect.
 
When iron levels decline below optimal thresholds, it can disrupt thermoregulatory mechanisms, leading to alterations in body temperature.
One of the primary functions of iron is its participation in the synthesis of hemoglobin, the protein responsible for transporting oxygen from the lungs to tissues throughout the body. Oxygen consumption is intricately linked to metabolic heat production, whereby cells utilize oxygen to generate energy through cellular respiration. Consequently, inadequate iron levels can impair oxygen transport, limiting cellular energy production and subsequently reducing metabolic heat generation.
Beyond its influence on heat generation, iron deficiency can also affect thermoregulation by impairing heat dissipation mechanisms. Sweat glands, crucial for dissipating excess heat during periods of elevated body temperature, rely on adequate iron levels for optimal function. Iron deficiency can compromise sweat gland activity, diminishing the body's ability to dissipate heat efficiently. Consequently, individuals with low iron levels may experience difficulties in regulating body temperature, particularly during physical exertion or exposure to high ambient temperatures.

Furthermore, iron deficiency can disrupt thyroid function, exacerbating thermoregulatory dysfunction. Iron is essential for the synthesis of thyroid hormones, which play a central role in regulating metabolism and body temperature. Insufficient iron availability can impair thyroid hormone synthesis and function, leading to hypothyroidism characterized by a slowed metabolic rate and cold intolerance.

The consequences of impaired thermoregulation due to low iron levels extend beyond discomfort, potentially culminating in serious health complications. Prolonged exposure to suboptimal body temperatures can compromise immune function, increase susceptibility to infections, and exacerbate pre-existing health conditions. Additionally, individuals with iron deficiency may experience exacerbated symptoms of fatigue, lethargy, and cognitive impairment, further impeding their ability to cope with temperature fluctuations.
Can iron be supplemented? Or just eat more red meat or what?
 
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Not saying it was related to tirz but I was taking it at the time of this test last week. My blood markers have been skewed, mch,rdw and mchc. Been feeling run down, low energy, crappy sleep. Only on 200mg of test. Prob 3 blood dumps last year, not sure if that would have affected it.
 
See my iron (fer) and ferritine. First number is pre tirz and others 6 and 9 months after. The last number is after 3 months of supplmentation
 

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Not saying it was related to tirz but I was taking it at the time of this test last week. My blood markers have been skewed, mch,rdw and mchc. Been feeling run down, low energy, crappy sleep. Only on 200mg of test. Prob 3 blood dumps last year, not sure if that would have affected it.
That's why I love this board.
You get specific information for specific situations from real people that maybe had the same issues at some point and are villing to share their experience.
Thank you indeed...
 
View attachment 277855
Not saying it was related to tirz but I was taking it at the time of this test last week. My blood markers have been skewed, mch,rdw and mchc. Been feeling run down, low energy, crappy sleep. Only on 200mg of test. Prob 3 blood dumps last year, not sure if that would have affected it.
Each time you donate blood, you lose between 220-250 mg of iron. If you donate a Power Red, you lose twice that amount, about 470 mg of iron. It may take up to 24-30 weeks for your body to replace the iron lost through a blood donation. Source: Red Cross
 
Each time you donate blood, you lose between 220-250 mg of iron. If you donate a Power Red, you lose twice that amount, about 470 mg of iron. It may take up to 24-30 weeks for your body to replace the iron lost through a blood donation. Source: Red Cross
cool thanks I didn't realize how much iron is lost on a donation. I donate 3 times last year at the RC all about 8 weeks apart. My last donation there my hemoglobin was 13, while on 200mg of test. I was shocked it was never that low. I'm pretty confident that's the culprit of my low iron.
 
Interesting. Those on AAS compounds tend to see an increase in hematocrit values. Anyone using GLP-1 agonists concurrently - do you see a decrease in iron or other values?
 
While tirzepatide primarily targets glucose and weight regulation through its actions on the incretin system, some studies have suggested potential associations between glucagon-like peptide-1 (GLP-1) receptor agonists—such as tirzepatide—and alterations in iron metabolism. Specifically, GLP-1 receptor agonists have been implicated in the regulation of hepcidin, a key hormone involved in iron homeostasis. Hepcidin modulates iron absorption in the intestines and its release from storage sites, and dysregulation of hepcidin levels can lead to disturbances in iron metabolism.
Who the hell are you? You came bringing some knowledge as if you have been around a while. But I’ve never seen that handle before on any forums.

Regardless, thanks for the info. That will probably benefit many of us.
 

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