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Что уже было: http://healthy-back.livejournal.com/357868.html (август 2015)

Внизу этого поста поста - про генетику, наследственность и т.п.

Не могу найти ссылку мне оставляли на клинику где-то в Калифорнии. Там, в отличие от всяких Шрот-Шено, проводят анализ микронутриентов и нейротрансмиттеров. Поэтому размещаю то, что нашел поиском: https://www.treatingscoliosis.com/scoliosis-nutrition/

Предупреждаю сразу: советы избегать соль и жиры - идиотские и безграмотные, что, конечно, подрывает доверие.

Improved nutrition and supplements can help if your child has idiopathic scoliosis. Several studies have shown that nutritional deficiencies definitely have an influence on scoliosis, but nutrition's impact is poorly understood.

An unhealthy diet, low levels of specific minerals in the body, and hormone imbalances can all contribute to scoliosis progression. Poor nutrition doesn't cause idiopathic scoliosis, however. Children either have the gene or they don't. But, studies link the advancement of the condition to nutrition deficiencies.

Scoliosis is a genetic neuromuscular condition that may or may not progress. Typically, your child's brain would send messages to the muscles, telling them to straighten the spine as it grows. But when your child has scoliosis, the brain doesn't realize that the body's posture is not aligned, so it doesn't send these messages. This miscommunication — coupled with environmental factors like poor nutrition or certain sports — can trigger scoliosis progression.

Correcting Hormone Deficiencies Enhances Treatment

European studies link scoliosis progression with hormone deficiencies and the brain's lack of response to these hormones. These hormones include serotonin, melatonin, calmodulin, leptin, and growth hormones. The brain communicates with the body via neurotransmitters. Neurotransmitters have several functions in the brain, including controlling the flow of messages from the brain to the body. This flow of communication can be accelerated, delayed or blocked if your child's neurotransmitters are deficient.

We use scoliosis nutritional testing to find and correct hormone imbalances in your child. Since neurotransmitters are usually amino acids and specific B vitamins, supplements can fix most imbalances such as serotonin deficiencies. Serotonin is crucial for the body's proper dynamic postural control. Plus, the body converts serotonin into melatonin, which is another deficiency linked to scoliosis. Amino acids can correct both of these hormone imbalances. This enhances neuromuscular retraining that stops scoliosis progression. The ScoliSMART™ Auto Response Training program uses specific exercises to create new subconscious muscle memory. Nutritional support improves the results and endurance of this program.

Many Over-the-Counter Supplements Help Scoliosis

One study published by Wiley InterScience finds that many idiopathic scoliosis patients also have lower selenium levels than normal. Tests have also shown that scoliosis patients have high levels of a cytokine (a type of small protein) called Osteopontin (OPN), which regulates bone growth. If your child has a selenium deficiency, it may be causing high OPN levels and abnormal bone growth. Therapeutic doses of 200 micrograms of selenium (L-selenomethionine to be exact) can naturally decrease OPN levels and may slow or eliminate the risk of rapid scoliosis progression.

Other supplements to consider after nutritional screening include:

Inflavonoids. These herbal pain relievers combine Ayurvedic herbs such as ginger and turmeric with lemon bioflavonoids and vitamin C. The anti-inflammatory herbs help keep the body’s stress response down, while the vitamin C helps support the muscles and connective tissue that hold the spine in place.

Digestive aids. A digestive enzyme formula such as Metagest (or Metaxyme for those who prefer a vegetarian supplement) can help counteract the digestive problems that often accompany scoliosis. A probiotic that promotes healthy bacteria in the intestine is also useful for supporting digestive health.

EPA-DHA Complex. These omega-3 fatty acids play a critical role in helping the brain function and build gray matter. Since scoliosis is caused by a breakdown in communication between the brain and muscles, effective treatment requires retraining the brain to correct postural defects — and omega-3s help support this process.

Probioplex. This probiotic and protein blend promotes healthy bacteria in the intestine, which ultimately promotes bone health. Some types of gut bacteria affect the way the body metabolizes sex hormones, leading to a loss of bone density.

Collagenics. This unique combination of free-form amino acids, key minerals and other nutrients helps support healthy connective tissue, which aids in the development of postural strength.

Vitamin D3. Vitamin D plays an essential role in helping the body absorb calcium, which is necessary for increasing bone density. It also supports the metabolism as well as neurological functions.

Multigenics. This blend of vitamins, calcium and amino acids improves liver health and adrenal function. A healthy liver allows the absorption of bone-building vitamins D, E, K and A — plus it produces key enzymes that help transport nutrients.

With the right diet and nutritional supplements, patients with scoliosis can boost the effectiveness of treatment while eliminating some of the factors that spur the condition’s progression.

Improving Overall Diet is Also Key for Scoliosis Support

In addition to correcting your child's hormone and nutritional imbalances, you can also improve your family's diet to support your child and reduce the risk of scoliosis progression. These diet suggestions are good for anyone, with or without scoliosis.

Eating foods that are low in nutrients or loaded with chemical additives and preservatives can result in nutritional deficiencies and cause chronic inflammation. Inflammation is a stress response that causes the body to release cytokines, which cause bone loss. Its toll on your bones is so high that people with high indicators for inflammation suffer 73 percent more hip fractures. It also depletes your muscles — and weak muscles have a much harder time holding the spine in position.

Additionally, many of these foods deprive the bones and muscles of nutrients necessary for the effective treatment of scoliosis. For example, salt causes excessive calcium excretion through the kidneys, while sugar and soda inhibit the body’s ability to absorb calcium. Alcohol contributes to low bone mass and limits bone formation, while caffeine actually leaches calcium from bones at the rate of 6 milligrams of lost calcium for every 100 milligrams of caffeine ingested.

Doctors also recommend limiting citrus fruits and juices (including tomato juice), whose citric acid can cause the body to move calcium from the bones to the blood, causing the skeletal structure to weaken.

It may seem overwhelming to eliminate all of the foods and additives linked to both poor health and scoliosis progression. Start by reading labels. You may not realize where salt, sugar and additives are hiding in your food. Then, look for healthier substitutes, such as whole-grain flours instead of white flour. Buy organic fruits and vegetables as often as possible. Non-organic foods often have pesticides, carcinogens, hormone disruptors, neurotoxins, and developmental toxins linked to health problems and disease.

И сразу: https://www.treatingscoliosis.com/scoliosis-causes/
What Causes Scoliosis?
A Spinal Curve is just the Symptom of Brain/Muscle Miscommunication


The postural control centers are in the hind brain, in the same area that controls many other automatic body functions like breathing, heart rate and digestion. Like posture, none of these functions are voluntarily controlled. Spinal posture is an automatic neurological orientation to gravity that most of us take for granted.

If you or your child has scoliosis, these control centers aren't alerting the central nervous system and muscles of the abnormal posture, so the spine curves instead of correcting itself. The spinal muscles aren't weak, which is a common misconception; they just aren't getting the right messages.

Weak muscles don't lead to scoliosis curve progression, either. Curve progression appears to be largely dependent on genetic and environmental influences ranging from nutritional deficiencies to specific athletic activities. Your child may be genetically predisposed to severe scoliosis (curves that progress to over 45 degrees) or may have a mild case that's not likely to advance. The genetic test called ScoliScore™ accurately predicts curve progression in each person, which is a great advancement in treating scoliosis.

Additional factors drive curve progression after curves reach 20 degrees. As scoliosis progresses, it twists and bends the spine around its axis. This increased torque forces more twisting and bending. Imagine what a rubber band looks like when you twist it and it kinks in the middle. We have to stop this torque to stop the spinal deformity because it's a self-feeding loop.

Клиника в Нью Йорке (штате, не городе) выкладывает нам статью про гормоны. Оригинал статьи: https://link.springer.com/article/10.1007/s00264-015-2742-6
Клиника предлагает нам почитать: http://www.hudsonvalleyscoliosis.com/what-causes-scoliosis-scoliosis-and-hormones/
Connection Between Adolescent Idiopathic Scoliosis (AIS) and Puberty

К сожалению, только про девочек. Очевидно, мальчики - еще большая загадка. Гормоны надпочечников или щитовидной железы никого не интересуют. Банального тестостерона или функции ЖКТ тоже нет.

Scoliosis (spinal curvature) in adolescents is one of the most frequent forms of postural distortion and it occurs predominately in pubescent girls. The authors theorize that because of this, one of the many factors that may contribute to the expression of AIS must involve a significant deficiency of estrogens (the hormones that become active and trigger the onset of puberty).

Researchers tested concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH) , estrogens, progesterone, osteocalcin, RANKL and the activity of alkaline phosphatase (AP) in prepubescent and post pubescent scoliotic girls and compared them to samples taken from non-scoliotic pre and post pubescent girls. Before we discuss the outcome, here is breakdown of what was tested and how each functions within the body.

What was tested?

Follicle-Stimulating Hormone Regulates the development, growth, pubertal maturation and reproductive processes of the body. FSH and LH act synergistically in reproduction.
Luteinizing Hormone Produced by gonadotroph cells in the anterior pituitary gland. In females, an acute rise of LH triggers ovulation. LH and FSH levels rise and fall together during the monthly menstrual cycle.
Estradiol One of several natural estrogens. Predominant during reproductive years. Regulates menstrual cycles.
Estrone Least abundant of the three estrogens, Estrone converts to estrone sulfate, a long-lived derivative. Estrone sulfate acts as a reservoir that can be converted as needed to the more active estradiol. It is the predominant estrogen in postmenopausal women.
Estriol One of several natural estrogens. Abundant primarily during pregnancy.
Progesterone Involved in the menstrual cycle, pregnancy, and embryogenesis. Progesterone levels are relatively low during the preovulatory phase of the menstrual cycle, rise after ovulation, and are elevated during the luteal phase. Progesterone levels are relatively low in children and postmenopausal women.
Alkaline Phosphatase A byproduct of osteoblast activity. ALP increases if there is active bone formation. Levels are significantly higher in children and pregnant women.
Osteocalcin Secreted solely by osteoblasts and thought to play a role in the body’s metabolic regulation and is pro-osteoblastic (bone-building).
RANKL Receptor activator of nuclear factor kappa-B ligand. Through the binding of RANKL, osteoclasts and osteoblasts play a vital role in normal bone remodeling. Overproduction of RANKL is associated with a number of degenerative bone diseases (e.g. rheumatoid arthritis and psoriatic arthritis)



What were their findings?

In premenarcheal scoliotic girls, the levels of FSH, LH and estradiol were lower; the levels of progesterone, estrone and estriol were higher; and the concentrations of estrone and estriol were similar compared to girls without scoliosis. Higher levels of RANKL, osteocalcin and AP were observed in premenarcheal adolescents with AIS compared with non-scoliosis.

In postmenarcheal Scoliotic girls, the levels of FSH, LH, estradiol, and progesterone were lower, estrone were slightly lower and estriol did not differ compared with postmenarcheal girls without scoliosis. Significantly higher levels of RANKL, osteocalcin and AP were observed in postmenarcheal scoliotic adolescents compared with non-scoliosis.

Their research revealed that the levels of FSH, LH, and estradiol in premenarcheal girls with AIS were markedly lower than in girls without scoliosis. The levels of FSH, LH, estradiol, and estrone in postmenarcheal girls with AIS were also lower compared to girls without scoliosis. They suggest that such findings can be explained by delayed puberty. The average age of girls with scoliosis was higher in both the pre- and postmenarcheal groups compared to the groups without scoliosis.

Levels Compared to Groups of Girls without Scoliosis
FSH
LH
Estrone
Estriol
Estradiol
Progesterone
AP
Osteocalcin
RANKL
Premenarcheal Scoliotic Girls
lower
lower
similar to control
similar to control
lower
higher
higher
higher
higher
Postmenarcheal Scoliotic Girls
lower
lower
slightly lower
same
lower
higher
higher
higher
higher


As the authors state, there is already plenty of research that supports a multifactorial cause of scoliosis and (as we’ve discussed in previous articles) the involvement of genetic and epigenetic predispositions and the influence of hormonal factors are also widely accepted. Scoliosis is assumed to be associated with a sex-linked predominant gene with incomplete penetrance (meaning that symptoms are not always present in individuals who have the genetic mutation) and variable expression (meaning variations in type and severity of a genetic disorder can exist between individuals with the same genetic mutation, even within the same family).

There are twice as many girls with Cobb angles greater than 10° and eight times as many with Cobb angles greater than 30°. Are hormones the only reason AIS occurs more frequently in girls than boys? The article references another study from 2012 that explains how Adolescent idiopathic scoliosis occurs between 2-10 times more frequently in females than in males with the Carter effect. In this situation males would need to inherit a greater number of susceptibility genes (compared to females) in order to develop AIS. They would also be more likely to pass scoliosis to their children and to have siblings with AIS. In the families they tested, AIS was lowest in sons of affected mothers (36%) and highest in daughters of affected fathers (85%). Fathers with scoliosis transmitted AIS to 80% of the children in the test, whereas mothers transmitted it to 56%. There was also significantly higher prevalence of AIS (55%) in siblings of males with scoliosis compared with siblings of females with scoliosis (45%). They suggest that this presentation of the Carter effect supports the “multifactorial threshold model of inheritance in AIS”.

What role might estrogen play in Scoliosis formation?

It is believed that AIS develops in two stages: initial functional impairment of osteoblasts and osteoclasts (which control the amount of bone tissue: osteoblasts form bone, osteoclasts repair/remodel bone), and the stage of actual spinal deformation. However, the reason, like so much of scoliosis, is still unknown.

Estrogens influence bone growth and remodeling, and control changes in the structure of cancellous bones (spongy bone). The authors are not suggesting that estrogens cause AIS, but that due to their function, they may affect progression. Estrogen deficiency is associated with increased bone turnover, increased osteoclast and osteoblast activity. Estrogens also control the activity of the melatonin receptor and inhibit the synthesis of melatonin. They interact with other hormones and biochemical factors, such as calcium-binding protein calmodulin, as well as with other proteins controlling muscle contractility.
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