Agenda Tersembunyi Telah Terjadi Pada Dunia Kesehatan di Indonesia Sesuai Dengan Pidato Bapak Presiden Prabowo Subianto
(A Hidden Agenda Has Occurred in the World of Health in Indonesia According to President Prabowo Subianto's Speech)
Kami akan menjelaskan kenapa Indonesia mengalami kegagalan dalam pelayanan kesehatan. Teori fokal infeksi dokter umum telah dihilangkan oleh oknum akademisi kedokteran diindonesia, dengan mengadopsi teori teori baru yang ternyata masih belum layak untuk menggantikan teori fokal infeksi dokter umum, berhubung  masih banyak ketidak jelasan dan ketidak tahuan yang mendasari teori baru tersebut. Penyakit fokal infeksi (infeksi bakteri dimukosa yang menahun) adalah penyebab utama masalah kesehatan diindonesia, dan menjadi penyebab utama kerusakan organ pada bangsa Indonesia. Akan tetapi teori ini telah disingkirkan oleh oknum oknum akademisi kedokteran diindonesia (dokter spesialis) melalui kolegium IDI dengan dalih kemunculan teori baru yang ternyata jauh dari harapan terhadap kebenaran teorinya.
(We will explain why Indonesia is experiencing a failure in healthcare services. The focal infection theory of general practitioners has been dismissed by certain medical academics in Indonesia, adopting new theories that are still inadequate to replace the focal infection theory of general practitioners, due to the many uncertainties and misunderstandings underlying the new theory. Focal infection disease (chronic bacterial infection in the mucosa) is a major cause of health problems in Indonesia and a major cause of organ damage in the Indonesian nation. However, this theory has been dismissed by certain medical academics in Indonesia (specialists) through the Indonesian Doctors Association (IDI) collegium, under the pretext of the emergence of a new theory that turns out to be far from the truth of the theory.)
Dibawah ini adalah penjelasan singkat mengenai teori fokal infeksi dokter umum :
(Below is a brief explanation of the general practitioner's theory of focal infection)
Contoh contoh infeksi bakteri di mukosa yang menahun : infeksi gigi dan gusi, infeksi mukosa usus (TBC usus, ulkus gaster/helikobakter pilori, typhoid/tifes yang hampir perforasi/jebol), radang paru (termasuk TBC paru), tonsilitis, sinusitis, infeksi telinga tengah, ambeien/wasir, infeksi menular seksual, infeksi saluran kencing. (Examples of chronic bacterial infections in the mucosa: tooth and gum infections, intestinal mucosa infections (intestinal tuberculosis, gastric ulcers/Helicobacter pylori, typhoid/typhus that is almost perforated/ruptured), pneumonia (including pulmonary tuberculosis), tonsillitis, sinusitis, middle ear infections, hemorrhoids, sexually transmitted infections, urinary tract infections)
Kenapa sering menahun? Karena kesalahan persepsi, contoh infeksi gigi dan gusi yang sudah menahun hingga syarafnya mati dan tidak nyeri, si pasien akan menganggap tidak sakit gigi dan gusi padahal gusinya sudah bernanah. Infeksi TBC usus, ulkus gaster (Helicobacter pilori), tifes (typhoid) yg hampir perforasi/jebol, dianggap cuma sakit maag saja, padahal sudah disertai meriang, terjadi berulang tiap bulan, dan sudah bertahun - tahun (seharusnya endoskopi). TBC paru dianggap sakit asma, padahal wheezingnya karena infeksi pneumonia dan tidak bilateral. Kondisi ini akan membuat seseorang akan mengalami infeksi bakteri dimukosa yang bertahun tahun dan akan sering larut dalam darah bakteri maupun potongan bakterinya (toxin). (Why is it often chronic? Due to misperceptions, for example, tooth and gum infections that have persisted for years until the nerves are dead and painless, the patient will assume there is no tooth or gum pain when in fact the gums are already festering. Intestinal tuberculosis infections, gastric ulcers (Helicobacter pylori), typhus (typhoid) that is almost perforated/ruptured, are considered just stomach ulcers, even though they are accompanied by chills, occur repeatedly every month, and have been for years (an endoscopy should be performed). Pulmonary tuberculosis is considered asthma, even though the wheezing is due to pneumonia infection and is not bilateral. This condition will cause a person to experience bacterial infections in the mucosa for years and will often dissolve in the blood of bacteria or pieces of bacteria (toxins))
Kondisi ini juga membuat kesalahan persepsi berupa kelainan genetik/keturunan dengan dukungan teori baru yang masih belum jelas dan belum diketahui. Dengan adanya kesalahan persepsi diatas oleh orang tua, tentu akan mengajarkan kepada anaknya tentang penyakit tersebut yang menimbulkan kesalahan persepsi yang sama. Ditambah lagi adanya dukungan teori teori baru dokter spesialis  yang hanya menunjukkan perubahan genetic dan bukan kelainan genetik, sebab masih dalam kategori adaptasi sel saja. Orang tua yang mengalami sakit, salah persepsi seperti contoh diatas, kemudian mengajarkan kepada anaknya sehingga mengalami hal yang sama dengan orang tuanya dan dianggap sebagai masalah genetik, ditambah lagi dukungan dari kesalahan penelitian yang masih dalam kategori perubahan genetic akibat adaptasi sel saja, tetapi dinyatakan sudah menjadi kelainan genetic. Contohnya, TBC dianggap kelainan genetik, dimana orang dalam keluarga yang TBC dianggap asma saja oleh orang tuanya, kemudian anaknya juga menganggap asma juga, dan didukung kesalahan dokter yang tidak mampu membedakan wheezing akibat asma atau akibat infeksi, bahkan wheezing yang tidak bilateral, dianggap bukan pneumonia, sehingga anak dan ibu akan didiagnosa asma. Akhirnya satu keluarga telah mengalami TBC. Semua kondisi diatas, menyebabkan pembiaran infeksi bakteri dimukosa menahun dalam keluarga. Pembiaran fokal infeksi akan menyebabkan penyakit penyakit organ yang dialami dalam satu keluarga tersebut, seperti hipertensi akibat sensitive garam (padahal karena ketidakmampuan kompensasi ginjal akibat fokal infeksi menahun), gagal ginjal IgAN, penyakit jantung coroner, miokarditis, infark miokard, pembesaran jantung, vasculitis pembuluh darah besar, diabetes, aneurysma/stroke, dan thyroiditis. Dan anehnya, kelainan organ yang terjadi akibat pembiaran penyakit fokal infeksi dalam satu keluarga tadi, apabila mengalami penyakit yang sama, tetap akan dihubung hubungkan juga sebagai akibat kelainan genetic/keturunan oleh dokter spesialis dengan memunculkan teori teori baru yang cuma menunjukkan perubahan genetic akibat adaptasi sel saja, tetapi sudah dinyatakan masuk dalam kategori kelainan genetic (cacat genetic). Jadi terlihat pola penyakit yang disebabkan oleh infeksi bakteri mukosa menahun (fokal infeksi) dialihkan dengan menghubung - hubungkan penyebabnya oleh kelainan genetic, sampai komplikasi organ akibat fokal infeksi pun dihubungkan dengan kelainan genetic juga. (This condition also creates misperceptions in the form of genetic/hereditary disorders, supported by new theories that are still unclear and unknown. With these misperceptions, parents will certainly teach their children about the disease, which leads to the same misperceptions. Furthermore, there is support for new theories from specialist doctors that only point to genetic changes and not genetic disorders, because they are still categorized as cell adaptation. Parents who experience the disease, with misperceptions like the example above, then teach their children, who experience the same experience as their parents and are considered genetic problems. This is further supported by research errors that still categorize genetic changes due to cell adaptation, but are declared genetic disorders. For example, tuberculosis is considered a genetic disorder, where the person in the family with tuberculosis is considered only asthma by the parents, then the child also thinks it has asthma. This is supported by the error of doctors who are unable to differentiate wheezing due to asthma from infection, even wheezing that is not bilateral is considered not pneumonia, so the child and mother are diagnosed with asthma. Ultimately, the entire family has TB. All of the above conditions lead to the neglect of chronic bacterial mucosal infections in the family. Ignoring a focal infection will cause organ diseases experienced by the same family, such as hypertension due to salt sensitivity (even though it is due to the inability of the kidneys to compensate due to chronic focal infection), IgAN kidney failure, coronary heart disease, myocarditis, myocardial infarction, heart enlargement, large vessel vasculitis, diabetes, aneurysm/stroke, and thyroiditis. And strangely, organ disorders that occur due to neglecting the focal infection disease in the same family, if experiencing the same disease, will still be linked to the cause of genetic/hereditary disorders by specialists who have come up with new theories that only show genetic changes due to cell adaptation, but have been declared to be included in the category of genetic disorders (genetic defects). So it seems that the pattern of disease caused by chronic mucosal bacterial infections (focal infections) is shifted by linking the cause to genetic disorders, until organ complications due to focal infections are also linked to genetic disorders.)
Ciri khas fokal infeksi yaitu infeksi bakteri di mukosa bertahun tahun dan berulang - ulang proses akutnya, maka akan menimbulkan seringnya penyebaran secara hematogen dengan respon (The characteristic of focal infection is bacterial infection in the mucosa for years and the acute process is repeated, which will result in frequent hematogenous spread with an inflammatory response):
- Respon immun berupa IgA (karena berasal dari infeksi dimukosa), limfosit dan makrofag tanpa atau sedikit respon netrofil dan belum menjadi sepsis. (The immune response consists of IgA (because it originates from mucosal infection), lymphocytes and macrophages with no or little neutrophil response and has not yet become sepsis)
- Respon komposisi darah berupa terbentuknya albumin agregat, aglutinasi, thrombus hingga peningkatan profil lipid. (The blood composition response includes the formation of aggregate albumin, agglutination, thrombus and increased lipid profile)
- Respon dinding pembuluh darah akibat penempelan bakteri/potongan bakteri berupa terjadi tahap - tahap perubahan dari normal menjadi tonus berkurang, kaku (seringnya penempelan bakteri/bakterial fragmen), penebalan hingga sklerosis. (The response of the blood vessel wall due to the attachment of bacteria/bacterial fragments is in the form of stages of change from normal to reduced tone, stiffness (often due to the attachment of bacteria/bacterial fragments), thickening to sclerosis)
- Respon messenger kimia berupa messenger kimia yang berasal dari sel hingga messenger kimia yang berasal dari sisa residu sel darah putih (akibat sekresi enzyme lysosome/sitotoksik termasuk akibat sekresi enzyme lisosom sebelum fagositosis sempurna akibat terlalu banyak vakuola fagositosis dalam sel/makrofag). (Chemical messenger responses include chemical messengers originating from cells to chemical messengers originating from residual white blood cells (due to the secretion of lysosome/cytotoxic enzymes, including the secretion of lysosome enzymes before complete phagocytosis due to too many phagocytic vacuoles in cells/macrophages).
- Respon sisa residu dari respon radang berupa produk sisa yg netral, produk sisa yg bersifat Radikal bebas seperti oxLDL dan produk sisa berupa messenger kimia. (The residual response from the inflammatory response is in the form of neutral waste products, free radical waste products such as oxLDL and waste products in the form of chemical messengers)
Perjalanan penyakit fokal infeksi (infeksi bakteri dimukosa menahun) ketika larut dalam darah, ternyata menimbulkan kesalahan persepsi juga. Kulit mukosa tidak memiliki lapisan lemak, berbeda dengan kulit dermis (kulit luar kita) yang terdapat lapisan lemak dibawahnya. Lapisan lemak inilah yang membuat infeksi bakteri pada dermis sangat sulit larut dalam darah, berbeda dengan infeksi bakteri pada mukosa. Bakteri dan bakterial fragmen/LPS/potongan bakteri pada mukosa kemudian larut dalam darah, akan membuat/mengikat albumin menjadi albumin aggregate (hasil lab akan meningkatkan LED), teraglutinasi, mengikat lipoprotein (protein pembawa lemak) seperti HDL, LDL dan sebagainya (hasil lab akan meningkatkan profil lipid dan meningkatkan sekresi empedu akibat lipid tidak bisa didistribusikan dan banyak yang dimetabolisme oleh hati), teraglutinasi dan memudahkan bakteri/potongan bakteri beserta perubahannya menempel pada permukaan pembuluh darah bagian dalam (lumen) dan merusaknya. Peningkatan profil lipid ini, disalah artikan selama ini akibat pengaruh makanan, gaya hidup dan sebagainya, padahal penyebabnya karena bakteri yang larut dalam darah dan berikatan dengan liporotein. Albumin aggregate (albumin yg berikatan dengan potongan bakteri), bila dipakai oleh plasenta untuk membuat struktur janin, maka ibu hamil akan menjadi preeklampsia termasuk eclampsia hingga menimbulkan kecacatan pada bayi (termasuk gangguan perkembangan organ). Seringnya penempelan bakteri/bakterial fragmen/LPS pada dinding pembuluh darah, lama kelamaan akan membuat perubahan dari normal menjadi tonus berkurang, kaku, penebalan, hingga sclerosis. Semua itu sering disebabkan oleh fokal infeksi akan tetapi literatur dokter spesialis menyatakan akibat penyebab lain selain fokal infeksi. (The course of focal infectious disease (chronic bacterial infection in the mucosa) when dissolved in the blood, apparently also causes misperceptions. The skin of the mucosa does not have a layer of fat, unlike the skin of the dermis (our outer skin) which has a layer of fat underneath. This layer of fat makes bacterial infections in the dermis very difficult to dissolve in the blood, unlike bacterial infections in the mucosa. Bacteria and bacterial fragments/LPS/bacterial pieces in the mucosa then dissolve in the blood, will create/bind albumin into albumin aggregates (lab results will increase ESR), agglutinate, bind lipoproteins (fat-carrying proteins) such as HDL, LDL and so on (lab results will increase the lipid profile and increase bile secretion because lipids cannot be distributed and many are metabolized by the liver), agglutinate and make it easier for bacteria/bacterial pieces and their changes to attach to the surface of the inner blood vessels (lumen) and damage them. This increase in lipid profile has been misinterpreted as being due to the influence of food, lifestyle, and so on. However, the cause is actually bacteria that dissolve in the blood and bind to lipoproteins. Albumin aggregate (albumin bound to pieces of bacteria), when used by the placenta to build fetal structure, can cause preeclampsia, including eclampsia, which can cause birth defects (including impaired organ development). The frequent attachment of bacteria, bacterial fragments, and LPS to blood vessel walls will eventually cause changes from normal to reduced tone, stiffness, thickening, and even sclerosis. All of these are often caused by focal infections, but specialist medical literature states that they are caused by causes other than focal infections)
