My @Quora answer to Should parents have their children vaccinated? Why, or why not? http://qr.ae/7mGL93
Here’s your answer:
You want the best for your kid right? So let’s be logical here in trying to give them the BEST ODDS for a long and happy life.
1) Consider: IF (note that this is a large and hotly disputed if)… IF vaccines cause these problems the occurrence is LESS THAN 0.001%.
2) Actual odds on getting a disease that we’re vaccinating for (especially considering we’ve already had outbreaks of mumps and measels)
On the order of 0.1% with the herd immunity we have had. Of we lose or give up that herd immunity from all being vaccinated that number rises by a few orders of magnitude.
3) Now… go look up what these do to their victims as kids AND as adults. I’ll help.
4) Also, consider: The Autism “link” just MIGHT be due to the 30 fold increase in toxins from our industrially farmed “foods” look up glyphosphate, nicotinoids, malthion, alar, and other pesticides… my suspicion? IMO these are the true core and cause of the “problem”.
Glycophosphate is a proven endocrine disruptor which the USDA just increased the allowance of residue for BY OVER TWO TIMES THE OLD “SAFE” LEVEL. For no better reason than corporate “convenience”, and profits. They did this with zero review and zero (mandated) Public Comment Period.
These diseases and chemicals MAIM AND KILL!
So: Which action offers you kid the BEST ODDS (since that’s all we can do for them) for a long, healthy, happy, life?! :
Italicized text is what you are risking for YOUR child by not vaccinating them:
Death is very unusual. The disease is self-limiting, and general outcome is good, even if other organs are involved. Known complications of mumps include:
Infection of other organ systems
Mumps viral infections in adolescent and adult males carry an up to 30% risk that the testes may become infected (orchitis or epididymitis), which can be quite painful; about half of these infections result in testicular atrophy, and in rare cases sterility can follow.
Spontaneous abortion in about 27% of cases during the first trimester of pregnancy.
Mild forms of meningitis in up to 10% of cases (40% of cases occur without parotid swelling)
Oophoritis (inflammation of ovaries) in about 5% of adolescent and adult females, but fertility is affected in almost half of these 5%.
Pancreatitis in about 4% of cases, manifesting as abdominal pain and vomiting
Encephalitis (very rare, and fatal in about 1% of the cases when it occurs)
Profound (91 dB or more) but rare sensorineural hearing loss, uni- or bilateral. Acute unilateral deafness occurs in about 0.005% of cases.
After the illness, lifelong immunity to mumps generally occurs; reinfection is possible but tends to be mild and atypical.
The majority of patients survive measles, though in some cases complications may occur, which may include bronchitis, and—in about 1 in 100,000 cases—panencephalitis, which is usually fatal. The patient may spread the disease to an immunocompromised patient, for whom the risk of death is much higher, due to complications such as giant cell pneumonia. Acute measles encephalitis is another serious risk of measles virus infection. It typically occurs two days to one week after the breakout of the measles exanthem and begins with very high fever, severe headache, convulsions and altered mentation. A patient may become comatose, and death or brain injury may occur.
In 2011, the WHO estimated that there were about 158,000 deaths caused by measles. This is down from 630,000 deaths in 1990. Death occurs, in developed countries, in about 1 in 1,000 cases (.1%). In populations with high levels of malnutrition and a lack of adequate healthcare, mortality can be as high as 10%. In cases with complications, the rate may rise to 20–30%. Increased immunization has led to a 78% drop in measles deaths which made up 25% of the decline in mortality in children under five.
Rubella infection of children and adults is usually mild, self-limiting and often asymptomatic. The prognosis in children born with CRS is poor.
Rubella is a disease that occurs worldwide. The virus tends to peak during the spring in countries with temperate climates. Before the vaccine to rubella was introduced in 1969, widespread outbreaks usually occurred every 6–9 years in the United States and 3–5 years in Europe, mostly affecting children in the 5-9 year old age group. Since the introduction of vaccine, occurrences have become rare in those countries with high uptake rates.
Vaccination has interrupted the transmission of rubella in the Americas: no endemic case has been observed since February 2009. Since the virus can always be reintroduced from other continents, the population still need to remain vaccinated to keep the western hemisphere free of rubella. During the epidemic in the US between 1962–1965, Rubella virus infections during pregnancy were estimated to have caused 30,000 still births and 20,000 children to be born impaired or disabled as a result of CRS. Universal immunisation producing a high level of herd immunity is important in the control of epidemics of rubella.
In the UK, there remains a large population of men susceptible to rubella who have not been vaccinated. Outbreaks of rubella occurred amongst many young men in the UK in 1993 and in 1996 the infection was transmitted to pregnant women, many of whom were immigrants and were susceptible. Outbreaks still arise, usually in developing countries where the vaccine is not as accessible.
On January 22, 2014, the World Health Organization and the Pan American Health Organization declared and certified Colombia free of the rubella and became the first Latin American country to abolish the disease within its borders.
Rubella was first described in the mid-eighteenth century. Friedrich Hoffmann made the first clinical description of rubella in 1740, which was confirmed by de Bergen in 1752 and Orlow in 1758.
In 1814, George de Maton first suggested that it be considered a disease distinct from both measles and scarlet fever. All these physicians were German, and the disease was known as Rötheln (contemporary German Röteln), hence the common name of “German measles”. Henry Veale, an English Royal Artillery surgeon, described an outbreak in India. He coined the name “rubella” (from the Latin word, meaning “little red”) in 1866.
It was formally recognised as an individual entity in 1881, at the International Congress of Medicine in London. In 1914, Alfred Fabian Hess theorised that rubella was caused by a virus, based on work with monkeys. In 1938, Hiro and Tosaka confirmed this by passing the disease to children using filtered nasal washings from acute cases.
In 1940, there was a widespread epidemic of rubella in Australia. Subsequently, ophthalmologist Norman McAllister Gregg found 78 cases of congenital cataracts in infants and 68 of them were born to mothers who had caught rubella in early pregnancy. Gregg published an account, Congenital Cataract Following German Measles in the Mother, in 1941. He described a variety of problems now known as congenital rubella syndrome (CRS) and noticed that the earlier the mother was infected, the worse the damage was. The virus was isolated in tissue culture in 1962 by two separate groups led by physicians Parkman and Weller.
There was a pandemic of rubella between 1962 and 1965, starting in Europe and spreading to the United States. In the years 1964-65, the United States had an estimated 12.5 million rubella cases. This led to 11,000 miscarriages or therapeutic abortions and 20,000 cases of congenital rubella syndrome. Of these, 2,100 died as neonates, 12,000 were deaf, 3,580 were blind and 1,800 were mentally retarded. In New York alone, CRS affected 1% of all births 
Denervation of skeletal muscle tissue secondary to poliovirus infection can lead to paralysis.
In around 1% of infections, poliovirus spreads along certain nerve fiber pathways, preferentially replicating in and destroying motor neurons within the spinal cord, brain stem, or motor cortex. This leads to the development of paralytic poliomyelitis, the various forms of which (spinal, bulbar, and bulbospinal) vary only with the amount of neuronal damage and inflammation that occurs, and the region of the CNS affected.
The destruction of neuronal cells produces lesions within the spinal ganglia; these may also occur in the reticular formation, vestibular nuclei, cerebellar vermis, and deep cerebellar nuclei. Inflammation associated with nerve cell destruction often alters the color and appearance of the gray matter in the spinal column, causing it to appear reddish and swollen. Other destructive changes associated with paralytic disease occur in the forebrain region, specifically the hypothalamus and thalamus. The molecular mechanisms by which poliovirus causes paralytic disease are poorly understood.
Early symptoms of paralytic polio include high fever, headache, stiffness in the back and neck, asymmetrical weakness of various muscles, sensitivity to touch, difficulty swallowing, muscle pain, loss of superficial and deep reflexes, paresthesia (pins and needles), irritability, constipation, or difficulty urinating. Paralysis generally develops one to ten days after early symptoms begin, progresses for two to three days, and is usually complete by the time the fever breaks.
The likelihood of developing paralytic polio increases with age, as does the extent of paralysis. In children, nonparalytic meningitis is the most likely consequence of CNS involvement, and paralysis occurs in only one in 1000 cases. In adults, paralysis occurs in one in 75 cases. In children under five years of age, paralysis of one leg is most common; in adults, extensive paralysis of the chest and abdomen also affecting all four limbs—quadriplegia—is more likely. Paralysis rates also vary depending on the serotype of the infecting poliovirus; the highest rates of paralysis (one in 200) are associated with poliovirus type 1, the lowest rates (one in 2,000) are associated with type 2.
The location of motor neurons in the anterior horn cells of the spinal column
Spinal polio, the most common form of paralytic poliomyelitis, results from viral invasion of the motor neurons of the anterior horn cells, or the ventral (front) grey matter section in the spinal column, which are responsible for movement of the muscles, including those of the trunk, limbs, and the intercostal muscles. Virus invasion causes inflammation of the nerve cells, leading to damage or destruction of motor neuron ganglia. When spinal neurons die, Wallerian degeneration takes place, leading to weakness of those muscles formerly innervated by the now-dead neurons. With the destruction of nerve cells, the muscles no longer receive signals from the brain or spinal cord; without nerve stimulation, the muscles atrophy, becoming weak, floppy and poorly controlled, and finally completely paralyzed. Maximum paralysis progresses rapidly (two to four days), and usually involves fever and muscle pain. Deep tendon reflexes are also affected, and are typically absent or diminished; sensation (the ability to feel) in the paralyzed limbs, however, is not affected.
The extent of spinal paralysis depends on the region of the cord affected, which may be cervical, thoracic, or lumbar. The virus may affect muscles on both sides of the body, but more often the paralysis is asymmetrical. Any limb or combination of limbs may be affected—one leg, one arm, or both legs and both arms. Paralysis is often more severe proximally (where the limb joins the body) than distally (the fingertips and toes).
The location and anatomy of the bulbar region (in orange)
Making up about 2% of cases of paralytic polio, bulbar polio occurs when poliovirus invades and destroys nerves within the bulbar region of the brain stem. The bulbar region is a white matter pathway that connects the cerebral cortex to the brain stem. The destruction of these nerves weakens the muscles supplied by the cranial nerves, producing symptoms of encephalitis, and causes difficulty breathing, speaking and swallowing. Critical nerves affected are the glossopharyngeal nerve (which partially controls swallowing and functions in the throat, tongue movement, and taste), the vagus nerve (which sends signals to the heart, intestines, and lungs), and the accessory nerve (which controls upper neck movement). Due to the effect on swallowing, secretions of mucus may build up in the airway, causing suffocation. Other signs and symptoms include facial weakness (caused by destruction of the trigeminal nerve and facial nerve, which innervate the cheeks, tear ducts, gums, and muscles of the face, among other structures), double vision, difficulty in chewing, and abnormal respiratory rate, depth, and rhythm (which may lead to respiratory arrest). Pulmonary edema and shock are also possible and may be fatal.
Approximately 19% of all paralytic polio cases have both bulbar and spinal symptoms; this subtype is called respiratory or bulbospinal polio. Here, the virus affects the upper part of the cervical spinal cord (cervical vertebrae C3 through C5), and paralysis of the diaphragm occurs. The critical nerves affected are the phrenic nerve (which drives the diaphragm to inflate the lungs) and those that drive the muscles needed for swallowing. By destroying these nerves, this form of polio affects breathing, making it difficult or impossible for the patient to breathe without the support of a ventilator. It can lead to paralysis of the arms and legs and may also affect swallowing and heart functions.
Here’s more dangers (as if the above weren’t enough)
Glycophosphate or Roundup
Roundup Herbicide Causes Smorgasbord of Fatal Diseases, New Study Concludes
The Horrific Truth About Monsanto’s Roundup Herbicide
Monsanto’s Roundup Herbicide May Be Most Important Factor in Development of Autism and Other Chronic Disease
Neonicotinoids, Malathion, Alar, and other pesticides.
Autism and Agricultural Pesticides: Integrating Data to Track Trends
Pesticide Exposure and Risk of Autism
Please use your brain for all our sakes.
Note: I am NOT a doctor and this is not medical advice.