2. Stabilize islet cell membrane and help islet cells recover their original secretory function.
Scavenge free radicals on the surface of red blood cells, enhance their compliance and oxygen-carrying ability, make red blood cells carry more oxygen to exchange with islet cells, and reduce the secretion of glucagon in islet A cells.
4 prevent the oxidation of low density lipoprotein LDL to Ox-LDL, increase high density lipoprotein HDL and improve atherosclerosis in small and medium-sized arteries.
In view of the increasing number of outpatients seeking advice on diabetes and anti-oxidation, combined with the understanding of astaxanthin and the clinical application experience in recent two years, this paper discusses some problems of long-term use of astaxanthin and short-term use of insulin to treat diabetes, which is also recommended by ADA (American Diabetes Association). The pathology of type 2 diabetes is non-infectious subacute inflammation caused by excessive oxidative damage. The root cause of type 2 diabetes is islet overload or islet aging. In order to restore the islet to normal state, it is necessary to reduce the burden of islet. Traditional treatment methods of diabetes, such as diet adjustment, exercise, insulin injection or administration, biguanides, acarbose, etc., are all good methods to reduce the burden of islets and belong to palliative measures. However, it is not enough to reduce the burden, but also to remove the factors that continue to damage the islet to restore its function. This is an effective "antioxidant stress". This is the root cause. Long-term use of strong antioxidants such as astaxanthin (ASTA) and short-term use of insulin can be called treating both the symptoms and root causes. The program has achieved remarkable clinical results in the past two years, and some diabetic patients have completely got rid of insulin injection.
Can 1。 Does astaxanthin treat diabetes?
This question is somewhat similar to: Can penicillin treat pneumonia? As a doctor, objectively speaking, effective anti-infection can cure pneumonia. Similarly, effective anti-oxidation can effectively prevent and treat type 2 diabetes and treat a series of complications caused by diabetes. Because the pathological basis of type 2 diabetes is non-infectious and subacute series inflammatory reactions caused by excessive oxidative stress.
That sounds a little awkward. Everyone knows that diabetes is divided into 1 type and type 2, and 1 type diabetes can only be treated with insulin according to the current medical level. The type of insulin resistance in type 2 diabetes (90%) can be completely cured by effective antioxidants such as astaxanthin. Unfortunately, many patients with type 2 diabetes have delayed treatment because they have not adopted the correct treatment method!
How to judge whether my diabetes is 1 or 2?
This problem is not complicated. When insulin or C-peptide is tested in the hospital, it can be clear whether it is 1 type or type 2, or whether it is insulin resistance type. Insulin-resistant diabetics secrete a lot of insulin. Some may be higher than normal people, and insulin secretion may be delayed after meals. What does this mean? This shows that the "islet" organ is still functional, that is, when we are tired, our tissues are insensitive to insulin or secrete more glucagon. For example, the previous treatment was: the island was already very tired after running. At this time, if you whip it quickly and whip it a few times, the horse will run faster, but it will soon be exhausted. The drug that stimulates insulin secretion is this "whip". Therefore, this whip can't be whipped at this time. At this time, exogenous insulin should be used for a short time to rest the islets. However, this does not solve the fundamental problem, and it is necessary to remove those factors that continue to damage islet β cells, such as oxygen free radicals, which can directly damage DNA, protein and lipids, and can also be used as functional molecular signals to activate various stress-sensitive signaling pathways in cells, which are closely related to insulin resistance and the impairment of β cell function. Only by removing these harmful components can islet cells recover, and the process of removing these harmful components is anti-oxidation. As scientists say: oxidative damage is the mother of all injuries. Therefore, effective anti-oxidation can restore islet β cells. Only in this way can islet A cells correctly identify the blood sugar level and reduce the secretion of glucagon, so that even if insulin secretion is very small, blood sugar can be reduced.
. . . . . See further reading 1. The mechanism of astaxanthin and gout is to prevent gout effectively by inhibiting the oxidative decomposition of nucleic acid and the oxidation of purine to uric acid.
It is a well-known fact that the cause of gout is related to blood uric acid, but what causes the increase of uric acid and purine is unknown. The main reason of high uric acid is abnormal purine metabolism. A large number of purines are oxidized to (2.6.8 trioxypurine) in the liver, which is called uric acid. However, many patients do not eat seafood, touch their internal organs, drink beer, basically do not eat high-purine food, do not exercise, and their blood uric acid is still rising. Why on earth is this?
This is because every cell in our body has a lot of DNA or RNA, that is, we have a lot of nucleic acid in our body. As shown above, the double-stranded structure of DNA contains a lot of adenine (a) and guanine (g). The nucleus is mainly DNA, and the cytoplasm is mainly RNA. All protein (such as enzyme), immunoglobulin, etc. The synthesis of protein requires RNA transcription and information transmission. Therefore, nucleic acid exists in any active cell in our body. In the process of continuous oxidative decomposition and replication, RNA and DNA are oxidized and decomposed when attacked by free radicals or in the process of self-aging, which means that purine is the waste of DNA and RNA oxidation.
Biochemistry tells us that both DNA and RNA are nucleic acids composed of gene fragments, mainly composed of phosphoric acid and five base pairs, namely, A (adenine), T (thymine), C (cytosine) and G (guanine) U (uracil). So when the nucleic acid is decomposed by oxidation, almost half of the bases are purines. Therefore, even if you don't eat purine foods, if nucleic acids are constantly oxidized, you will produce high concentrations of purine, which will also lead to an increase in blood uric acid, which explains why middle-aged and elderly men who don't eat purine foods will produce a lot of blood uric acid because of the existence of peroxidation in their bodies.
In addition, 70% gout patients without high uric acid, 8-OHdG (nucleic acid oxidation marker) will increase. Therefore, after finding out the cause of gout, in the treatment of gout, effectively inhibiting the oxidative decomposition of nucleic acid can effectively inhibit the production of endogenous purines and effectively prevent gout and hyperuricemia.
. . . . . . For patients with acute cerebral infarction, such as urokinase and streptokinase. It is used to dissolve thrombus within 3 hours, which is medically called RT-PA therapy and can be recanalized quickly and effectively. However, no matter which method is used to treat cerebral infarction, the recurrence rate of cerebral infarction is still high, with the incidence rate of about 30% in the first 30 days. The first arterial infarction after treatment usually occurs within 7- 10 days after treatment. How to prevent the recurrence of cerebral infarction has become the biggest headache for neurologists and patients.
There used to be two methods: 1. Extend the use time of thrombolytic enzyme to about 65438 00 days. One of the risks of overusing thrombolytic enzymes is that it may lead to cerebral hemorrhage, because many patients with cerebral infarction are suffering from heart disease, atrial fibrillation, hypertension and atherosclerosis, and their blood vessels are very fragile. 2. Use some antiplatelet drugs such as aspirin and dipyridamole, but the harm of long-term use of these drugs is to cause coagulation dysfunction. The so-called coagulation dysfunction means that it is difficult to eliminate ecchymosis if you accidentally hit it, or it is difficult to stop bleeding from the wound. Of course, if there is cerebral hemorrhage, it is equally difficult to stop bleeding.
However, a study from the United States gave a new method, that is, taking a large dose of astaxanthin (ASTA)20-24mg/ day (5-6 capsules/day) can effectively prevent the recurrence of cerebral infarction, while not affecting the body's coagulation function and avoiding the risk of cerebral hemorrhage. Patients with hypertension can also be used as drugs for long-term prevention of cerebral infarction. The existing evidence shows that oxidative stress and its inflammatory reaction are the mechanism of abnormal thrombosis, and astaxanthin has powerful antioxidant and anti-inflammatory effects, so it can effectively inhibit the process of "oxidative stress" and control the inflammatory reaction in the process of thrombosis to some extent. Therefore, it can effectively inhibit the formation of arterial thrombosis. Greatly reduce the chance of re-infarction.
The recent X-ray diffraction technology clearly shows that astaxanthin can maintain the structure of cell membrane and show super antioxidant activity, while β -carotene interferes with the normal structure of cell membrane and shows extremely low antioxidant activity. The difference of these antioxidants in cell membrane can easily explain why non-polar antioxidants such as β-carotene, vitamin E and vitamin C have not achieved clinical success.
The above judgment has also been supported by our clinic. On the third day after thrombolysis, patients with cerebral infarction began to take astaxanthin (ASTA)20-24mg/ day and stopped using anticoagulants. After two months, the consumption of astaxanthin is reduced to 12mg/ day, which can effectively avoid the recurrence of cerebral infarction in patients with cerebral infarction.
. . . . . . See further reading 3.