The recent discussion of ASPS and lactate got the best of my curiousity
Type" could lactate play a role in cachexia " and came upon a just released article
could Ammonium lactate cause Cachexia?
http://www.ehealthme.com/ds/ammonium%2Blactate/cachexia
cachexia
http://jnci.oxfordjournals.org/content/89/23/1763.full
Could Ammonium lactate cause Cachexia?
Biology of Cachexia
Biology of Cachexia
Abstract
About half of all cancer patients show a syndrome of cachexia, characterized by loss of adipose tissue and skeletal muscle mass. Such patients have a decreased survival time, compared with the survival time among patients without weight loss, and loss of total body protein leads to substantial impairment of respiratory muscle function. These changes cannot be fully explained by the accompanying anorexia, and nutritional supplementation alone is unable to reverse the wasting process. Despite a falling caloric intake, patients with cachexia frequently show an elevated resting energy expenditure as a result of increases in Cori cycle (i.e., catalytic conversion of lactic acid to glucose) activity, glucose and triglyceride-fatty acid cycling, and gluconeogenesis. A number of cytokines, including tumor necrosisfactor-α, interleukins 1 and 6, interferon γ, and leukemia-inhibitory factor, have been proposed as mediators of the cachectic process. However, the results of a number of clinical and laboratory studies suggest that the action of the cytokines alone is unable to explain the complex mechanism of wasting in cancer cachexia. In addition, cachexia has been observed in some xenograft models even without a cytokine involvement, suggesting that other factors may be involved. These probably include catabolic factors, which act directly on skeletal muscle and adipose tissue and the presence of which has been associated with the clinical development of cachexia. A polyunsaturated fatty acid, eicosapentaenoic acid, attenuates the action of such catabolic factors and has been shown to stabilize the process of wasting and resting energy expenditure in patients with pancreatic cancer. Such a pharmacologic approach may provide new insights into the treatment of cachexia.
The word “cachexia” is derived from the Greek “kakos” meaning “bad” and “hexis” meaning “condition.” It occurs in a number of disease states, including cancer, acquired immunodeficiency syndrome (AIDS), major trauma, surgery, malabsorption, and severe sepsis. Cachexia is characterized by weight loss involving depletion of host adipose tissue and skeletal muscle mass. Weight loss in cancer patients differs from that found in simple starvation. During the first few days of starvation, glucose utilization by the brain and erythrocytes necessitates depletion of liver and muscle glycogen and an increased glucose production by the liver, using gluconeogenic amino acids derived from catabolism of muscle. This early phase is replaced in long-term starvation by the use of fat as a fuel, in which free fatty acids released from adipose tissue are converted into ketone bodies, which are utilized for energy by peripheral tissues and eventually to a great extent by the brain. This leads to conservation of muscle mass. In anorexia nervosa, more than three quarters of the weight loss arises from fat and only a small amount from muscle. In contrast, in cancer cachexia, there is equal loss of both fat and muscle, so that for a given degree of weight loss there is more loss of muscle in a patient with cachexia than in a patient with anorexia nervosa ( 1 ). Thus, although anorexia is common in cancer patients, with reports of occurrence in 15%–40% of subjects at presentation ( 2 ), the body composition changes suggest that anorexia alone is not responsible for cachexia. Also, in malnourished cancer patients, the measured food intake fails to correspond with the degree of malnutrition ( 3 ), and loss of both muscle and adipose tissue has been reported to precede the fall in food intake ( 4 ). In contrast to simple starvation, it is not possible to reverse the body composition changes seen in patients with cancer cachexia by the provision of extra calories. Attempts to increase energy intake in cancer patients through dietary counseling failed to reverse the cachexia ( 5 ). Trials of total parenteral nutrition in cachectic cancer patients also failed to show benefit in terms of increased median survival time or long-term weight gain ( 6 ). Although a short-term weight gain was observed, this weight was subsequently lost, suggesting the retention of water ( 7 ). Analysis of body composition indicated that patients receiving total parenteral nutrition temporarily maintained body fat stores, but there was no evidence for preservation of lean body mass. Thus, the cause of wasting in cancer cachexia is more complex than that in simple starvation.
https://academic.oup.com/jnci/article/8 ... 63/2526545
Abstract
About half of all cancer patients show a syndrome of cachexia, characterized by loss of adipose tissue and skeletal muscle mass. Such patients have a decreased survival time, compared with the survival time among patients without weight loss, and loss of total body protein leads to substantial impairment of respiratory muscle function. These changes cannot be fully explained by the accompanying anorexia, and nutritional supplementation alone is unable to reverse the wasting process. Despite a falling caloric intake, patients with cachexia frequently show an elevated resting energy expenditure as a result of increases in Cori cycle (i.e., catalytic conversion of lactic acid to glucose) activity, glucose and triglyceride-fatty acid cycling, and gluconeogenesis. A number of cytokines, including tumor necrosisfactor-α, interleukins 1 and 6, interferon γ, and leukemia-inhibitory factor, have been proposed as mediators of the cachectic process. However, the results of a number of clinical and laboratory studies suggest that the action of the cytokines alone is unable to explain the complex mechanism of wasting in cancer cachexia. In addition, cachexia has been observed in some xenograft models even without a cytokine involvement, suggesting that other factors may be involved. These probably include catabolic factors, which act directly on skeletal muscle and adipose tissue and the presence of which has been associated with the clinical development of cachexia. A polyunsaturated fatty acid, eicosapentaenoic acid, attenuates the action of such catabolic factors and has been shown to stabilize the process of wasting and resting energy expenditure in patients with pancreatic cancer. Such a pharmacologic approach may provide new insights into the treatment of cachexia.
The word “cachexia” is derived from the Greek “kakos” meaning “bad” and “hexis” meaning “condition.” It occurs in a number of disease states, including cancer, acquired immunodeficiency syndrome (AIDS), major trauma, surgery, malabsorption, and severe sepsis. Cachexia is characterized by weight loss involving depletion of host adipose tissue and skeletal muscle mass. Weight loss in cancer patients differs from that found in simple starvation. During the first few days of starvation, glucose utilization by the brain and erythrocytes necessitates depletion of liver and muscle glycogen and an increased glucose production by the liver, using gluconeogenic amino acids derived from catabolism of muscle. This early phase is replaced in long-term starvation by the use of fat as a fuel, in which free fatty acids released from adipose tissue are converted into ketone bodies, which are utilized for energy by peripheral tissues and eventually to a great extent by the brain. This leads to conservation of muscle mass. In anorexia nervosa, more than three quarters of the weight loss arises from fat and only a small amount from muscle. In contrast, in cancer cachexia, there is equal loss of both fat and muscle, so that for a given degree of weight loss there is more loss of muscle in a patient with cachexia than in a patient with anorexia nervosa ( 1 ). Thus, although anorexia is common in cancer patients, with reports of occurrence in 15%–40% of subjects at presentation ( 2 ), the body composition changes suggest that anorexia alone is not responsible for cachexia. Also, in malnourished cancer patients, the measured food intake fails to correspond with the degree of malnutrition ( 3 ), and loss of both muscle and adipose tissue has been reported to precede the fall in food intake ( 4 ). In contrast to simple starvation, it is not possible to reverse the body composition changes seen in patients with cancer cachexia by the provision of extra calories. Attempts to increase energy intake in cancer patients through dietary counseling failed to reverse the cachexia ( 5 ). Trials of total parenteral nutrition in cachectic cancer patients also failed to show benefit in terms of increased median survival time or long-term weight gain ( 6 ). Although a short-term weight gain was observed, this weight was subsequently lost, suggesting the retention of water ( 7 ). Analysis of body composition indicated that patients receiving total parenteral nutrition temporarily maintained body fat stores, but there was no evidence for preservation of lean body mass. Thus, the cause of wasting in cancer cachexia is more complex than that in simple starvation.
https://academic.oup.com/jnci/article/8 ... 63/2526545
Debbie
A Case Report of Reversal of Cancer Cachexia and Literature Review.. Huaixing M*, Li P and Suyi L Department of Oncology
A Case Report of Reversal of Cancer Cachexia and Literature Review
Huaixing M*, Li P and Suyi L
Department of Oncology Nutrition and Metabolic Therapy, The First Affiliated
Abstract
Cancer cachexia, as a special malnutrition, has poor efficacy with nutritional support alone. Patients with cachexia are likely to experience reduced quality of life and survival. Timely and effective intervention can reverse cachexia and improve the clinical outcome of patients. This patient was diagnosed as esophageal cancer, accompanied by cachexia, esophageal fistula, anemia and hypoproteinemia. After combination therapy, including nutritional support, metabolic regulation, anti-tumor treatment and symptomatic treatment, the patient's symptoms were significantly relieved, and cachexia was reversed. The quality of life was improved tumor was significantly reduced.
Introduction
The clinical incidence of cancer cachexia is relatively high. Epidemiological study of more than 40,000 tumor patients in China shows that the incidence of cachexia is as high as 37% [1], which is higher in digestive system tumors than in other tumors. In another systematic review, the prevalence of 5-year cachexia at risk is estimated about 30% in all cancer patients in the USA and EU [2]. It is well known that cachexia is to be associated with decreased quality of life, reduced tolerance to anti-tumor therapy and reduced survival. Hence, there is a large unmet clinical need for therapy of cachexia. Most patients diagnosed esophageal cancer are already in locally advanced stage or have distant metastasis, and suffer from cachexia and various complications. Without timely and effective intervention, the quality of life and prognosis of those patients will be seriously affected [3]. As a special malnutrition state, cancer cachexia is characterized by persistent skeletal muscle loss, with or without loss of adipose tissue, often accompanied by anorexia, fatigue, anemia, hypoproteinemia, electrolyte imbalance, infection, etc. Meanwhile, it is accompanied by gradual damage to the functions of the heart, lungs and other organs. The pathophysiology is characterized by abnormal metabolism and negative balance of protein and energy caused by reduced intake. It is a multi-factor syndrome [4].
Cancer cachexia has its own characteristics and pathophysiological mechanism. It cannot be fully reversed by conventional nutritional support. However, cancer cachexia does not refer to the end-stage of the disease, but can occur in any stage of malignant tumor, including newly diagnosed, postoperative and end-stage patients. Timely and effective intervention can partially reverse the disease, and then improve the clinical outcome of such patients.
https://www.anncaserep.com/open-access/ ... e-9487.pdf
Huaixing M*, Li P and Suyi L
Department of Oncology Nutrition and Metabolic Therapy, The First Affiliated
Abstract
Cancer cachexia, as a special malnutrition, has poor efficacy with nutritional support alone. Patients with cachexia are likely to experience reduced quality of life and survival. Timely and effective intervention can reverse cachexia and improve the clinical outcome of patients. This patient was diagnosed as esophageal cancer, accompanied by cachexia, esophageal fistula, anemia and hypoproteinemia. After combination therapy, including nutritional support, metabolic regulation, anti-tumor treatment and symptomatic treatment, the patient's symptoms were significantly relieved, and cachexia was reversed. The quality of life was improved tumor was significantly reduced.
Introduction
The clinical incidence of cancer cachexia is relatively high. Epidemiological study of more than 40,000 tumor patients in China shows that the incidence of cachexia is as high as 37% [1], which is higher in digestive system tumors than in other tumors. In another systematic review, the prevalence of 5-year cachexia at risk is estimated about 30% in all cancer patients in the USA and EU [2]. It is well known that cachexia is to be associated with decreased quality of life, reduced tolerance to anti-tumor therapy and reduced survival. Hence, there is a large unmet clinical need for therapy of cachexia. Most patients diagnosed esophageal cancer are already in locally advanced stage or have distant metastasis, and suffer from cachexia and various complications. Without timely and effective intervention, the quality of life and prognosis of those patients will be seriously affected [3]. As a special malnutrition state, cancer cachexia is characterized by persistent skeletal muscle loss, with or without loss of adipose tissue, often accompanied by anorexia, fatigue, anemia, hypoproteinemia, electrolyte imbalance, infection, etc. Meanwhile, it is accompanied by gradual damage to the functions of the heart, lungs and other organs. The pathophysiology is characterized by abnormal metabolism and negative balance of protein and energy caused by reduced intake. It is a multi-factor syndrome [4].
Cancer cachexia has its own characteristics and pathophysiological mechanism. It cannot be fully reversed by conventional nutritional support. However, cancer cachexia does not refer to the end-stage of the disease, but can occur in any stage of malignant tumor, including newly diagnosed, postoperative and end-stage patients. Timely and effective intervention can partially reverse the disease, and then improve the clinical outcome of such patients.
https://www.anncaserep.com/open-access/ ... e-9487.pdf
Debbie
Re: Could Ammonium lactate cause Cachexia?
Feb 11,2017
D.ap wrote: ↑Sat Feb 11, 2017 10:47 pm Good morning all
Josh had his 15th infusion on Thursday and weighted in at a wapping 127.2 lbs!
His sleep patterns are still skewed but he is working on creating normal schedules with his day . Getting back to NORMAL is so challenging as you all can attest to today
Last year at this time we had been off sutent for 6 weeks after we had a " toxic" experience and discontinued after taking from end of September 2016 to November 24, 2016.
Josh was down to 95 pounds and was coughing pretty much night and day . He was suffering from
A) lack of Energy, drive
B) pain from broken rib after coughing fit while on sutinib
His over clinical physic had the doctors believing that he was possible succumbing to cachexia.
We explored having a stomach tube surgically installed so Josh could gain weight and consulted and incorporated a natural doctor and dietician into our care team .
Tumors were appearing in his lower cavity after the November discontinuation of sutent at an alarming rate .
( we all know that 1 can feel like an alarming rate . :| )
-June 19 Opdivo --weight 105 ish
-Aug 2016-- brain tumors started to disappear
-October-- lung,lower pelvic / cavity tumors reduced , inflammation i.e. Larger image of liver shown
-Jan 2017--weight 124.2
Liver reduction as well as other lower cavity tumors being followed
All brain tumors gone except LITT 1cm tumor that got all practical purposes is dead
Feb 9 weight 127.2
I know and understand there have been others before us on trial monoclonal and immune therapies who've had these excellent results . Who've given there lives with dose escalating trials . :cry: Our hearts and thanks needs to be said to these families .
That being said I also am being realistic in always being ahead of the game if at all possible in the event we need to change .
We as a family are so grateful for this extra year that has been given to us with Josh and look forward to many more! :P
Any suggestions are welcome
Love
Debbie
Debbie
Re: Could Ammonium lactate cause Cachexia?
It’s interesting to note that in 2015 we also had a non responsive brain tumor that was treated by LITT, after an unsuccessful SRS treatment.
In reading about cachexia there seems to be some association to traumatic brain injuries and hormones , that can be triggered by that event .
My limited understanding suggests that it can contribute to the hormal imbalance to ultimately be a basis of cachexia by virtue of the Adipokine gene?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2367125/
In reading about cachexia there seems to be some association to traumatic brain injuries and hormones , that can be triggered by that event .
My limited understanding suggests that it can contribute to the hormal imbalance to ultimately be a basis of cachexia by virtue of the Adipokine gene?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2367125/
The association of cachexia with TBI suggested the possible involvement of adipokines, such as leptin, that are well-known for their effects on appetite, bodyweight and energy metabolism
Debbie
Re: Could Ammonium lactate cause Cachexia?
“Leptin is an adipokine with central importance in the global obesity problem and consequent cardiovascular disease and is principally secreted by adipocytes and acts in the hypothalamus to suppress appetite and food intake, increase energy expenditure, and regulate body weight.”
https://cureasps.org/forum/viewtopic.php?f=53&t=951
https://cureasps.org/forum/viewtopic.php?f=53&t=951
Debbie