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Acid Reflux causes and Treatment

Peter Attia – The real cause of obesity (TED Talk Summary)

Peter Attia – The real cause of obesity (TED Talk Summary)

Despite exercising three or four hours every
single day and following the food pyramid to the letter, I gained a lot of weight and
developed metabolic syndrome. I had become insulin resistant and insulin resistance is
when your cells get increasingly resistant to effect of insulin trying to do its job.
You can think of insulin as this master hormone that controls what our body does with the
foods we eat, whether we burn it or store it. Once you’re insulin resistant, you’re
on your way to getting diabetes, which is what happens when your pancreas can’t keep
up with the resistance and make enough insulin. Now your blood sugar levels start to rise,
can lead to heart disease, cancer, even Alzheimer’s disease. I got busy changing my diet radically
– I did this and lost 40 pounds, as you can see, I guess I’m not overweight anymore, more
importantly I don’t have insulin resistance. Most researchers believe obesity is the cause
of insulin resistance. But what if we have it backwards? What if obesity isn’t the cause
of insulin resistance at all? In fact what if it’s a symptom of a much deeper problem?
What if obesity is a coping mechanism for a far more sinister problem going on underneath
the cell? You can think of insulin resistance as the reduced capacity of our cells to partition
fuel. Taking those calories that we take in and burning some appropriately and storing
some appropriately. When we become insulin resistant, the homeostasis in that balance
deviates, so now when insulin says to a cell “I want you to burn more energy” The cell
in effect says “No thanks, I’d actually rather store this energy” The appropriate response
to insulin resistance may actually to be to store it as fat. Not the reverse. What I’m
suggesting is maybe we have the cause and effect wrong on obesity and insulin resistance.
Is it possible that insulin resistance causes weight gain and the diseases assocaited with
obesity? At least in most people? We know that 30 million obese Americans in the United
States don’t have insulin resistance. Conversely, we know that 6 million lean people in the
United States are Insulin Resistant. They appear to be at even greater risk for those
metabolic diseases I mentioned a moment ago than their obese counter parts. If you can
be obese and not have insulin resistance and you can be lean and have it, this suggests
that obesity may just be a proxy. What a cell trying to protect itself from when it becomes
insulin resistant? It’s more likely too much glucose – blood sugar. We know that refined
grains and starches elevate your blood sugar in the short run; Might be our increased intake
of refined grains, sugars and starches that’s driving this epidemic of obesity and diabetes,
but through insulin resistance and not necessarily through just over eating and under exercising.
Our current beliefs about obesity, diabetes and insulin resistance could be wrong and
therefore must be tested.

2 Replies to “Peter Attia – The real cause of obesity (TED Talk Summary)”

  • Patients and treatments

    Case 1: The first patient was a 74 year old female with poorly controlled non-insulin- dependent diabetes, hypertension, and hypercholesterolemia. She was seen with vomiting, diarrhea and gangrene of second toe on left foot. Two weeks prior to admission, the patient had sustained fall in the bathroom resulting in a left ankle fracture with vomiting and diarrhea for seven days. The patient was treated with metformin and augmentin. Upon examination, the patient was afebrile with stable vital signs, and femoral pulses were present bilaterally. Popliteal and pedal pulses were absent bilaterally with poor capillary refill. The left foot was red and inflamed up to and including the medial malleolus. The lateral aspect of the great toe and second toe turned black. Laboratory investigation revealed elevated blood glucose (17.9 mmol/L) and hyponatremia (Na+ 128 mEg/L). The patient underwent a medial forefoot amputation as part of her management. Within 28 days after surgery, the 4th and 5th toes become discolored, dusky purple and black. The patient also developed a large blood blister over her heel. Vascular opinion was for a below knee amputation. The patient was self- discharged against medical advice. The patient was started on treatment by Electro Pressure Regeneration Therapy device (EPRT) while she was in hospital. She continued daily treatments on the EPRT device at home, along with a diabetic diet. The left foot continued to improve and heal, and her remaining gangrenous toes eventually fell off. Her blood pressure at admission was 166/53 with use of Lisinopril, which was dropped and eventually ceased as her BP continued to drop; 146/68, 129/64, 144/67 in second, third and fourth weeks after treatment, and to 128/66 during 6th to 8th weeks post-treatment while the patient was on no medication. Her blood sugar was improved and HbA1c was dropped from 9.8 before treatment to 7.6, 6.5, 5.9 and 5.5 during 9 months after commencement of treatment. The patient eventually stopped diabetic and hypertensive medications. To date her HbA1c remains below 6 on diet alone.

    Case 2: The second patient was a 65 year old male with a long history of non insulin dependent diabetes and hypertension. Diabetic neuropathy had affected his feet and he could not feel the shoe rubbing. A small superficial ulcer developed on his 5th toe which became infected and subsequently, the 5th toe was amputated. His condition rapidly deteriorated and he developed necrotizing fasciitis and osteomyelitis. Consequently, he had surgery removing tendons, skin and the capsular linings of joints from his right foot. The patient was discharged after ten weeks in hospital with a large, infected, open wound requiring community nurses to do wound management. The patient was treated by the Electro Pressure Regeneration Therapy device; the wound was healed completely without further management and the diabetes was well controlled. HbA1c dropped from 7.3 to 6.6 after treatment. His blood pressure was 202/99 before the treatment, which was dropped to 155/73 after two weeks. His blood pressure continued within normal range with the use of the Electro Pressure Regeneration Therapy device 2-3 times weekly.

    Case 3: A 70 year old female was diagnosed with hypertension, epilepsy osteoarthritis and rheumatoid arthritis. Her blood pressure was 147/84 which was dropped to 138/72 three weeks after the treatment with the Electro Pressure Regeneration Therapy device. She continued using the EPRT device twice weekly and her blood pressure was under control without the use of antihypertensive medications.

    Case 4: A 77 year old female with hypertension, hypercholesterolemia, hypothyroidism, and type 2 diabetes (NIDDM) was treated with the Electro Pressure Regeneration Therapy device. Her blood pressure before treatment was 158/81 which was dropped to 125/65 after 1 week. Her blood pressure continued to be normal with use of the EPRT device despite discontinuation of antihypertensive medications. HbA1c was 7.8 before treatment which decreased to 6.9 and continued to be low during one year follow-up.

    Case 5: A 67 year old female with hypertension and osteoarthritis was treated with the Electro Pressure Regeneration Therapy device. Her blood pressure was 157/91 which dropped to 149/86 after 3 weeks.

    Case 6: A 70 year old female with hypertension, fibromyalgia, hepatitis, hypercholesterolemia, tuberculosis and a stroke was treated with the Electro Pressure Regeneration Therapy device for her hypertension. Her blood pressure was 134/84 before treatment which was dropped to 117/73 within 4 weeks after treatment despite discontinuation of her antihypertensive medication.

    Case 7: A 75 year old female with hypertension and benign postural vertigo was treated with the Electro Pressure Regeneration Therapy device. Her blood pressure was 157/86 before treatment, which was dropped to 138/76 and continued within normal limits while receiving one treatment per week.

    Case 8: A 53 year old female with type 1 diabetes (IDDM) from the age of 12, suffered renal failure as a result of her diabetes and underwent a kidney and pancreatic transplant in 1994. She also has hypercholesterolemia, left ventricular failure, renal failure and a history of a coronary artery bypass graft. She then started treatment with the Electro Pressure Regeneration Therapy device. While she is not considered to currently have diabetes her HbA1c dropped over the time period she was receiving treatments from 5.4 to 5.1. This was matched by her Blood Sugar Level (BSL) which also stabilized while she was receiving treatment over this period of time.

    Case 9: A 32 year old female with type 1 diabetes (IDDM) and no other concurrent health problems was treated with the Electro Pressure Regeneration Therapy device. She received 8 treatments over a two week period. HbA1c before treatment was 8.1 and was dropped to 7.1 after treatment. Her insulin requirement was also reduced.

    Case 10: A 59 year old female with type 2 diabetes (NIDDM), hypertension, fibromyalgia, chronic active hepatitis, and Bowens disease was treated with the Electro Pressure Regeneration Therapy device. Her blood sugar was normalized and HbA1c dropped from 7.2 to 6.3 after the treatment. Her HbA1c showed a slight increase to 6.4 within three months after therapy was discontinued.

    Case 11: A 70 year old female with type 2 diabetes (NIDDM), osteoarthritis, chronic pain and multiple operations was treated with the Electro Pressure Regeneration Therapy device. Her average Blood Sugar Level (BSL) before treatment was 9.8, and dropped to 7.4 and 7.1 after three and six months of treatment. She was treated twice weekly with the EPRT device.

    Case 12: A 68 year old male with type 2 diabetes (NIDDM), hypertension, stroke, chronic pain and polio was treated with the Electro Pressure Regeneration Therapy device. HbA1c before treatment was 7.8, which was dropped to 6.6 during treatment. He was treated three times per week most weeks during a six month period. Upon discontinuation of therapy HbA1c increased to 7.8.

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