Swollen ankles/edema?

[Sophie7]

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[MikiSJ]

I had a period of time recently (last two months) where my feet and lower legs and hands had edema. I do not smoke, take finasteride and like you I don't add salt (except french fries ). Unlike you, I am not obese at #150/5'10".

I do have high blood pressure which is coming down under medication. I sit a lot in on chair while working at my desktop computer and I can relate, somewhat, that as being a cause.

Certainly is disconcerting when you can't get shoes on that fit yesterday, but not today.

[Kay]

Adding a small dose of Spiro, 25 mg-50 mg daily might help. Start with lower dose and adjust accordingly.

[Toku]

Lack of sleep contributes to it, definitely. I think the body produces stress hormones when you don't sleep and this can exacerbate it. Although I do not take E, if I ever exceed my "regular" T dose, the excess will convert to estrogen and cause edema, and if I've been missing sleep (like I had a couple of months back) the result is twice as bad. Water pills may help.

For now I figured out a dose in which there is no excess water retention, can gauge I'm normal by how bony the ankles feel.

[PentacleGoddess]

Something to talk to your doctor about as well. What's your sugar intake like? Edema can be indicative of diabetes too.

[Sophie7]

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[mitzidog]

I know it's a cliche, but do whatever is right for you, but you're right that you should speak to your doctor before making any changes to your meds.

[Kay]

I do not consume sugar, nor do I consume excessive amounts of saturated fat, which is actually the underlying cause of insulin resistance/prediabetes/diabetes/obesity.

Excess carbohydrates cause diabetes not saturated fat as the former stimulates insulin and chronically high levels of insulin result in insulin resistance.

[Sophie7]

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[Sophie7]

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[Kay]

And excess saturated fat intake spikes insulin far more than sugar intake. The reason for this is that the excess saturated fat gets inside the muscle cell, which prevents insulin from attaching to the muscle cell in order to allow the sugar into the muscle cell to be burned/metabolized. The pancreas then produces more insulin in an attempt to compensate for the fact that the rising insulin levels continually fail to get the job done.

It's like when you get home to your house and you can't get your key in the door because somebody put chewing gum in your lock. The lock is the muscle, the key is the insulin, the wad of gum is the fat, and you are the sugar trying to get in. Your pancreas keeps giving you more keys (more insulin) but none of them will work as long as the wad of chewing gum is there to block them.

There is empirical evidence to support this:

1) It has been observed using MRI technology.

2) All patients who decide to avoid abundant sources of saturated fats (oils, meat, eggs, dairy) have been shown to eliminate their diabetes symptoms- by removing the cause of the insulin resistance. In fact, these results are achieved on "high carb" diets that avoid processed foods and focus on carbohydrates in their natural forms, such as rice and potatoes.

I can see how you would think that sugars are the source of the problem. After all, there is a problem with blood sugar in such a situation. But that is speculative, reductionist thinking that has been disproven for several decades now. Scientists put people on an all-rice diets and all-potato diets, hypothesizing that it would make their diabetes worse. But instead, their diabetes went away and they became healthy, with no side effects or nutritional deficiencies (see link above).

Isn't that great?

Studies please. Only randomized controlled trials, no cohort or epidemiological studies from which no cause and effect can be clearly established.

https://nutritionandmetabolism.biomedce ... -7075-5-14

"We previously reported that a 20% carbohydrate diet was significantly superior to a 55–60% carbohydrate diet with regard to bodyweight and glycemic control in 2 groups of obese diabetes patients observed closely over 6 months (intervention group, n = 16; controls, n = 15) and we reported maintenance of these gains after 22 months."

"The initial mean HbA1c in 2003 in the low-carbohydrate group was 8.0 ± 1.5% (controls: 7.9 ± 1.5%). At the end of the 6 months study period it was 6.6 ± 1.0% (controls: 7.3 ± 1.8%), and after 12 months it was 7.0 ± 1.3%. It has since remained stable and is 6.8 ± 1.3% after 44 months."

"The effect of carbohydrate lowering on blood glucose was rapid. In the first week, mean fasting blood glucose dropped from 11.7 ± 3.3 mmol/l to 7.0 ± 1.4 mmol/l which necessitated corresponding reductions in medications."

"There is now little evidence for the claim that a fat-reduced diet for weight reduction has any particular value beyond caloric counting [10]. On the other hand, six randomised studies have shown that carbohydrate restriction with ad-libitum energy intake confers a significant benefit with regard to weight loss in obese persons [11, 12, 13, 14, 15, 16]. The current study is consistent with these reports and suggests that high-starch, high-carbohydrate diets excessively stimulate appetite and disturb energy balance in patients with the metabolic syndrome and type 2 diabetes [3]. A reduction of carbohydrates normalises the balance, reduces insulin concentrations and favours utilization of stored fat as fuel as well as significantly reducing insulin resistance [3]. Considering the solid evidence for the negative effect of hyperglycemia on diabetes complications as well as cardiovascular disease the present high-carbohydrate dietary advice resulting in unnecessary hyperglycemia and insulin resistance seems difficult to support [17, 18, 19] and for diabetes patients, current dietary recommendations seem to be a major part of their problem rather than being part of the solution. Carbohydrate restriction, however, reverses or neutralises all aspects of the metabolic syndrome [20, 21]."

"Summary: A reduced carbohydrate diet is effective in motivated patients and can be recommended for overweight patients with type 2 diabetes. There has been no sign of a negative cardiovascular effect."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1325029/

"The low-carbohydrate, ketogenic diet (LCKD) may be effective for improving glycemia and reducing medications in patients with type 2 diabetes."

"The LCKD improved glycemic control in patients with type 2 diabetes such that diabetes medications were discontinued or reduced in most participants. Because the LCKD can be very effective at lowering blood glucose, patients on diabetes medication who use this diet should be under close medical supervision or capable of adjusting their medication."

https://www.ncbi.nlm.nih.gov/pubmed/22673594

"Previous studies from our laboratory have shown the beneficial effects of a low-carbohydrate ketogenic diet (LCKD) in patients with type 2 diabetes after its long term administration. Furthermore, it favorably alters the cardiac risk factors even in hyperlipidemic obese subjects. These studies have indicated that, in addition to decreasing body weight and improving glycemia, LCKD can be effective in decreasing antidiabetic medication dosage."

"This study shows the beneficial effects of a ketogenic diet over the conventional LCD in obese diabetic subjects. The ketogenic diet appears to improve glycemic control."

LCD = low calorie diet

Samaha FF, et al. A low-carbohydrate as compared with a low-fat diet in severe obesity. New England Journal of Medicine, 2003.

"132 individuals with severe obesity (mean BMI of 43) were randomized to either a low-fat or a low-carb diet. Many of the subjects had metabolic syndrome or type II diabetes. The low-fat dieters were calorie restricted. Study duration was 6 months."

"The low-carb group lost significantly more weight (about 3 times as much). There was also a statistically significant difference in several biomarkers:

Triglycerides went down by 38 mg/dL in the LC group, compared to 7 mg/dL in the LF group.
Insulin sensitivity improved on LC, got slightly worse on LF.
Fasting blood glucose levels went down by 26 mg/dL in the LC group, only 5 mg/dL in the LF group.
Insulin levels went down by 27% in the LC group, but increased slightly in the LF group.
Overall, the low-carb diet had significantly more beneficial effects on weight and key biomarkers in this group of severely obese individuals."

Meckling KA, et al. Comparison of a low-fat diet to a low-carbohydrate diet on weight loss, body composition, and risk factors for diabetes and cardiovascular disease in free-living, overweight men and women. The Journal of Clinical Endocrinology & Metabolism, 2004

"Details: 40 overweight individuals were randomized to a low-carb and a low-fat diet for 10 weeks. The calories were matched between groups.

Weight Loss: The low-carb group lost 7.0 kg (15.4 lbs) and the low-fat group lost 6.8 kg (14.9 lbs). The difference was not statistically significant.

Conclusion: Both groups lost a similar amount of weight.

A few other notable differences in biomarkers:

Blood pressure decreased in both groups, both systolic and diastolic.
Total and LDL cholesterol decreased in the LF group only.
Triglycerides decreased in both groups.
HDL cholesterol went up in the LC group, but decreased in the LF group.
Blood sugar went down in both groups, but only the LC group had decreases in insulin levels, indicating improved insulin sensitivity."

https://www.ncbi.nlm.nih.gov/pubmed/19082851

"We recently proposed that the biological markers improved by carbohydrate restriction were precisely those that define the metabolic syndrome (MetS), and that the common thread was regulation of insulin as a control element. We specifically tested the idea with a 12-week study comparing two hypocaloric diets (approximately 1,500 kcal): a carbohydrate-restricted diet (CRD) (%carbohydrate:fat:protein = 12:59:28) and a low-fat diet (LFD) (56:24:20) in 40 subjects with atherogenic dyslipidemia. Both interventions led to improvements in several metabolic markers, but subjects following the CRD had consistently reduced glucose (-12%) and insulin (-50%) concentrations, insulin sensitivity (-55%), weight loss (-10%), decreased adiposity (-14%), and more favorable triacylglycerol (TAG) (-51%), HDL-C (13%) and total cholesterol/HDL-C ratio (-14%) responses. In addition to these markers for MetS, the CRD subjects showed more favorable responses to alternative indicators of cardiovascular risk"

"Despite a threefold higher intake of dietary saturated fat during the CRD, saturated fatty acids in TAG and cholesteryl ester were significantly decreased, as was palmitoleic acid (16:1n-7), an endogenous marker of lipogenesis, compared to subjects consuming the LFD. Serum retinol binding protein 4 has been linked to insulin-resistant states, and only the CRD decreased this marker (-20%). The findings provide support for unifying the disparate markers of MetS and for the proposed intimate connection with dietary carbohydrate. The results support the use of dietary carbohydrate restriction as an effective approach to improve features of MetS and cardiovascular risk."

https://www.ncbi.nlm.nih.gov/pubmed/24176230

"these findings demonstrate that individuals undergoing statin therapy experience additional improvements in metabolic and vascular health from a 6 weeks CRD as evidenced by increased insulin sensitivity and resistance vessel endothelial function, and decreased blood pressure, triglycerides, and adhesion molecules."

CRD = carb restricted diet (11% carbs, 58% fat)

https://www.ncbi.nlm.nih.gov/pubmed/19641727

"The present study shows the beneficial effects of a long-term ketogenic diet. It significantly reduced the body weight and body mass index of the patients. Furthermore, it decreased the level of triglycerides, LDL cholesterol and blood glucose, and increased the level of HDL cholesterol. Administering a ketogenic diet for a relatively longer period of time did not produce any significant side effects in the patients. Therefore, the present study confirms that it is safe to use a ketogenic diet for a longer period of time than previously demonstrated."

https://www.ncbi.nlm.nih.gov/pubmed/21978979

"High CHO intakes stimulate hepatic SAFA synthesis and conservation of dietary SAFA . Hepatic de novo lipogenesis from CHO is also stimulated during eucaloric dietary substitution of SAFA by CHO with high glycaemic index in normo-insulinaemic subjects and during hypocaloric high-CHO/low-fat diets in subjects with the metabolic syndrome. The accumulation of SAFA stimulates chronic systemic low-grade inflammation through its mimicking of bacterial lipopolysaccharides and÷or the induction of other pro-inflammatory stimuli. The resulting systemic low-grade inflammation promotes insulin resistance, reallocation of energy-rich substrates and atherogenic dyslipidaemia that concertedly give rise to increased CVD risk. We conclude that avoidance of SAFA accumulation by reducing the intake of CHO with high glycaemic index is more effective in the prevention of CVD than reducing SAFA intake per se."

CHO = carbohydrates
SAFA = saturated fatty acids
CVD = cardiovascular disease

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1208952/

"We believe restriction of saturated fat is not warranted on a low-carbohydrate diet because of our work showing favorable responses in clinical risk factors for diabetes and cardiovascular disease in low-carbohydrate diets that were rich in saturated fat [2]."

http://www.mensjournal.com/health-fitne ... t-20141020

"According to a new study from the National Institutes of Health, a diet that reduces carbohydrates in favor of fat – including the saturated fat in meat and butter – improves nearly every health measurement, from reducing our waistlines to keeping our arteries clear, more than the low-fat diets that have been recommended for generations. "The medical establishment got it wrong," says cardiologist Dennis Goodman, director of Integrative Medicine at New York Medical Associates. "The belief system didn't pan out."

"One year later, the high-fat, low-carb group had lost three times as much weight – 12 pounds compared with four – and that weight loss came from body fat, while the low-fat group lost muscle. Even more persuasive were the results of blood tests meant to measure the risk of heart disease and diabetes. The high-fat group, despite eating nearly twice as much saturated fat, still saw greater improvements in LDL cholesterol, HDL cholesterol, and triglycerides. This was enough to improve their scores on the Framingham Risk Calculator, a tool for predicting 10-year risk of heart attack. The low-fat group, by contrast, saw no improvement on their Framingham scores."

"When we eat carbs, they break down into sugar in the blood; that's true of whole grains, too, though to a lesser extent," says Jeff Volek, a leading low-carb researcher at Ohio State University. The body responds with the hormone insulin, which converts the extra blood sugar into fatty acids stored in the body fat around our middles. Our blood sugar then falls, and that body fat releases the fatty acids to burn as fuel. But carb-heavy diets keep insulin so high that those fatty acids aren't released, Volek says. The body continues to shuttle sugar into our fat cells – packing on the pounds – but we never burn it. Dietary fat, meanwhile, is the only macronutrient that has no effect on insulin or blood sugar. "This means it's likely excessive carbs, not fat, that plump us up," he adds. Low-carb diets stop that vicious cycle, keeping insulin levels low enough to force the body to burn fat again."

"The NIH report actually adds to research that's been accumulating for years. "It's something like the 25th clinical trial in the last 15 years to come out saying this, with almost none going the other way," says Westman."

[Kay]

Yes Kay, chronically high insulin levels indicate insulin resistance.

Not necessarily but they may lead to it.

And excess saturated fat intake spikes insulin far more than sugar intake.

You might find studies where there is an association (no cause and effect, people who eat lots of saturated fat might also be eating lots of sugar and processed foods) or studies in other animals (cannot be generalized to humans) but there are no randomized controlled placebo double blind trials where you will find that reducing saturated fat alone reduces insulin, fasting glucose and helps improve diabetes...none! In fact, I showed you several studies where carbs are lowered and despite more fat including saturated consumed, there were no deleterious effects and improvements. I think it's quite unequivocal.

The reason for this is that the excess saturated fat gets inside the muscle cell, which prevents insulin from attaching to the muscle cell in order to allow the sugar into the muscle cell to be burned/metabolized. The pancreas then produces more insulin in an attempt to compensate for the fact that the rising insulin levels continually fail to get the job done.

Has this mechanism been proven or is this speculation?

It's like when you get home to your house and you can't get your key in the door because somebody put chewing gum in your lock. The lock is the muscle, the key is the insulin, the wad of gum is the fat, and you are the sugar trying to get in. Your pancreas keeps giving you more keys (more insulin) but none of them will work as long as the wad of chewing gum is there to block them.

As far as I know, saturated fat does not bind to the insulin receptor. Please provide support for this.

There is empirical evidence to support this:

1) It has been observed using MRI technology.

Study please.

All patients who decide to avoid abundant sources of saturated fats (oils, meat, eggs, dairy) have been shown to eliminate their diabetes symptoms- by removing the cause of the insulin resistance. In fact, these results are achieved on "high carb" diets that avoid processed foods and focus on carbohydrates in their natural forms, such as rice and potatoes.

When you remove more than one thing in your diet and make several changes, you cannot establish clear cause and effect. It may be the reduction of processed foods containing abundant sugar that improved symptoms and not the removal of saturated fat.

I can see how you would think that sugars are the source of the problem. After all, there is a problem with blood sugar in such a situation. But that is speculative, reductionist thinking that has been disproven for several decades now.

In fact, it has been proven as studies earlier provided show.

Scientists put people on an all-rice diets and all-potato diets, hypothesizing that it would make their diabetes worse. But instead, their diabetes went away and they became healthy, with no side effects or nutritional deficiencies (see link above).

The link above is irrelevant. The all rice diet is not composed of rice exclusively but rather contain other foods such as fruits, veggies, beans, lean protein, etc. http://www.webmd.com/diet/a-z/rice-diet. The reason for improvement in health could be due to a reduction in overall sugar load and calorie restriction.

As far as the all potato diet, it's unhealthy long-term (nutritional deficiencies) and improvement short-term could also be due to the same reason, cutting down processed foods and reducing overall sugar content.

[brian24]

SPAM POST DELETED BY MODERATOR

[CALIGINA]

I suffered from that exact same thing (and sometimes the swelling went to my calves as well and even my whole legs, it looked real scary, my legs became huge in a matter of hours), when I was taking both estradiol and spironolactone, at their highest MTF-HRT dosages, pre-op.

After I had my male sexual glands removed, and stopped taking spironolactone, these incidents slowly stopped happening.

Then I added metformin, a Type 2 Diabetes drug useful for people with pre-diabetes or adult diabetes, which also happens to lower one's belly and waist fat.

After the combination of not taking spiro and taking metformin, I have never had any episodes of edema any more, not even when i keep sitting at my computer for more than four hours non-stop. And I don't even exercise anymore like I used to.

This is only my own real-life experience. You could visit an endocrinologist and get a professional assessment though. In my case, spiro was definitely the main reason for the problem, not estradiol, which I also happen to take sublingually as well.

Cheers

Gina