Temporal epidemiology
 

PD mortality rates, England and Wales, 1855-2004

Is there any evidence that the underlying prevalence of PD has increased over the last 150 years?

I cannot find any.

By underlying prevalence I mean the number of PwP taking into account changes in reporting conventions and practices, increasing population size, changes in the age distribution, the effects of drugs keeping people alive longer.

PD is usually under-repoted as a cause of death. The question is whether or not this is consistent.

What advantage does temporal epidemiology give?

If changes in prevalence could be linked to historical events, for instance the industrial revolution, that would be a major step to finding an aetiology for Parkinson's. As it is, no one heard the dog bark in the night. That, itself, is interesting.

Papers

A paper written nearly 50 years ago by Duvoisin and Schweitzer [1] gives some interesting insights into the rapid growth during the 19th and 20th centuries in the number of cases of PD, or paralysis agitans as it was known then.

Working from mortality data, the raw figures show a remarkable growth from an annual average for England and Wales of 21 cases in the latter half of the 1850s to 1600 by the start of the 1960s. This was a time of rising population, with people living longer. However, the authors put the main reason for the increase down to better reporting of the disease rather than higher real prevalence. But, as the authors point out, they cannot exclude that there was real growth.

A paper by Clarke [2] extends the period covered to 1989. The picture that he paints is the same: differences over time can be largely attributed to reporting changes and an ageing population. One difference that he points out, though, is that the introduction of levodopa extended the life expectancy of PwP by about 5 years.

A UK government report for the period 1979 to 2004 [3] reports:
"Mortality rates for mentions of Parkinson’s disease declined over the
period examined."
Again, this is thought to be due to PwP living longer.

References:

[1]"Paralysis Agitans Mortality in England and Wales, 1855-1962"
Duvoisin R., Schmeitzer M.
Brit. J. prev. soc. Med. (1966), 20, 27-33
http://pubmedcentralcanada.ca/pmcc/a...00081-0030.pdf

[2] "Mortality from Parkinson's disease in England and Wales 1921-89."
C E Clarke
J Neurol Neurosurg Psychiatry. 1993 June; 56(6): 690–693.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC489621/

[3] "Trends in mortality from Alzheimer’s disease, Parkinson’s disease and dementia, England and Wales, 1979–2004"
Griffiths C, Rooney C.
Office of National Statistics.
https://www.ons.gov.uk/ons/rel/hsq/h...-1979-2004.pdf

John

From back in the days when I thought I was writing a book-

PD is NOT an Old Disease!

Although first described in 1817 London, it is generally assumed that Parkinson’s Disease has long been a problem for humanity. This conclusion is usually based on a handful of ancient texts which describe an affliction characterized by tremor. But tremor is an initial manifestation of, not only PD, but a dozen other conditions. Observation in my own case and that of other PWP makes it clear that the defining symptoms of the later stages of our shared affliction, if untreated, would more likely be rigidity and slowness of movement (bradykinesia).

If that be so, then the texts, both before and after 1817, should be reflecting that. A man in the later stages would be more accurately described as “turned to stone” or some similar description of what we observe today. Yet, that is not so.

J. M. S. Pearce, in “Aspects of the History of Parkinson’s Disease” (1989), noted:

“Before James Parkinson's classic' "An Essay on the Shaking Palsy" (1817) ancient books recorded many types of paralytic disorders and tremors. None fully described the distinctive features of the syndrome which so justly perpetuates Parkinson's name.....

Pearce also noted:
“Trousseau's 15th Lecture on Clinical Medicine'° was on senile trembling and paralysis agitans. He described rigidity, a sign Parkinson did not pay attention to,,,”

Pearce’s own essay, published in the Journal of Neurology, Neurosurgery, and Psychiatry, unintentionally makes two important points:
Prior to 1817, the features of PD that we recognize today had not been of particular note; and
It was not until Trousseau’s 1868 lecture that rigidity was recognized as a symptom.

I will not attempt to reproduce Pearce’s work here nor is it necessary to do so in order to make my points. PD was not then nor is it now a well-defined, singular syndrome. Instead, it was, and remains, an amorphus and emerging condition that became noteworthy in the years just prior to Parkinson’s booklet in London where his observations were made.

In short, Parkinson’s Disease came into being as a result of the changes wrought by the Industrial Revolution. A number of symptoms define the later stages, but rigidity is one of the three primary ones (the others being slowness of motion and tremor) that define PD. Chronic rigidity is not easily overlooked by anyone involved with PD at any level. As such, it is a good marker for the disorder. And yet it is barely mentioned until the late 1800s..

Either our ancestors were very poor observers, or something else was going on. The former is almost laughable. What other possibilities are found in the latter that might lead to an explanation?

Both then and now, of PD is shown as a rapidly evolving disorder affecting multiple systems. It originated in the changes in London society during the great upheaval of the Industrial Revolution. Those changes are many, of course, but some seem particularly pertinent in light of what we experience as patients. Increased exposure to pollutants, for example. Others are more subtle. A shift from an agrarian lifestyle where stress tended to be acute and buffered by an extended family to an urban one where stress was chronic and worsened by the loss of the social safety net.

It is here that the origins of PD should be searched for.

1: Mov Disord. 1997 Nov;12(6):1068-72.

The shaking palsy, the first forty-five years: a journey through the British
literature.

Louis ED.

Department of Neurology, College of Physicians and Surgeons, Columbia University,
New York, New York, USA.

The authors examined the British medical literature published in the
45-year-period following Parkinson's treatise on the shaking palsy to determine
the number and type of references to the shaking palsy or paralysis agitans
during this particular period. Several sources suggest that Parkinson's 1817
treatise on the shaking palsy received little immediate attention in his native
country, England, and that not until 1861, in France, did Charcot began to
elucidate the clinical features of this entity, separating it from other
neurologic disorders (for example, multiple sclerosis). A review of the British
medical literature from the 45-year-period 1817-1861 revealed a number of
references to paralysis agitans, including those by Cooke (1820), Good (1824 and
1829), Elliotson (1827, 1829, 1830, 1831, and 1833), Gowry (1831), anonymous
(1832), Todd (1833), Watson (1836), Gibson (1839), Hall (1838 and 1841), Thompson
(1842), Graves (1843), Birkett (1853), Paget (1855), and Reynolds (1855). Many of
these did not report new or personally observed cases, did not separate
Parkinson's disease from other disease entities characterized by both "shaking"
and "palsy" (for example, tonic-clonic seizures), or misattributed motor signs to
dysfunction of the pyramidal system rather than an extrapyramidal system (that
is, attributing bradykinesia or rigidity to weakness). Although there were
several references to "shaking palsy" in the early- to mid-19th-century British
medical literature, there were few original case reports of Parkinson's disease.
This may have contributed to the fact that during this period little was added to
the original observations made by Parkinson in 1817. In particular, the
separation of bradykinesia and weakness did not become apparent until later work
by the French.


PMID: 9399240 [PubMed - indexed for MEDLINE]

Related Links

Unresolved issues relating to the shaking palsy on the celebration of James
Parkinson's 250th birthday. [Mov Disord. 2007] PMID:18175393

A new look at James Parkinson's Essay on the Shaking Palsy. [Neurology. 2007]
PMID:17664408

Charcot on Parkinson's disease. [Mov Disord. 1986] PMID:3332804

Lesions as therapy: rigidity and Parkinson's disease. [J Hist Neurosci. 2001]
PMID:11446268

[Johan Sebastian Welhaven's parkinsonism. An insight into the history of
literature] [Tidsskr Nor Laegeforen. 1995] PMID:8539742

Rick,

Thank you for your reply.

(What happened to the book?)

The key issue that you raise seems to me to be whether PD "started" in or about 1800. If I understand you correctly, you would argue in favour of this because, although tremors had been noted before, the combination of slowness, tremor and stiffness had not been.

A blogger [1] gives a number of examples from ancient civilizations of what may have been incidences of PD. He points out that:
"The Ayurveda’s description of kampavata includes tremors, stiffness, depression and a depletion of movement. The Ancient Indians prescribed a number of drugs to battle the symptoms of the disease, some of which scientists have come back to review today. These include the root of Withania somifera, the seed of Mucuna Pruriens Bak, Root of Sida Cordifolia and the fruit of Hyocyamus reticulatus".

I find this evidence compelling. So, I don't think that PD was new in 1800.

However, I hope you are right, because if we have a start date, this limits the number of pathogens that could be responsible for PD. London, and other cities were polluted before the Industrial Revoltion. So, I don't think that we should look for pollution in general as the culprit, but for something in particular that was added to the environment then. For example, a bit late, but aluminium was first isolated in 1827; there was an influenza epidemic in England in 1775-1776 [2].

The Industrial Revolution didn't happen in a day, there was a roll out of technologies and a move to urbanization that happened in different places at different times. If this is the case, we should see the same trends that happened in London around 1800 happen in other places later, indeed up to the present day.

References

[1] http://graecomuse.wordpress.com/2012...cient-history/

[2] http://en.wikipedia.org/wiki/List_of_epidemics

John

You are thinking too linearly when you speak of a "pathogen" as the cause. I maintain that PD is a state of being that reflects an ongoing collapse of a half-dozen critical systems with the closest thing to a "cause" being a hypervigilant immune system that overreacts to the ptesence of a very common substance (LPS) and which the regulation of the endocrine system is unable to handle. Its primary effect lies in the inflammatory response to the toxin, at least initially. But as life progresses, the triggering stimulus becomes more wide defined and includes anything which triggers or amplifies the neuro-inflammatory response. It doesn't matter if one is responding to the coal smoke of London in 1800 or of Mexico City in 2000 - IF one was exposed previously or even in utero to LPS. It is the reaction that is at the heart of PD and it is a bear because it feeds of so many sources.

Virtually every "cause" that has been put forward to evplain PD has ultimately failed after coming close initially. The research failed because it took into account only half the problem. There is a long list of these "failures" that suddenly spring back to life when the other half of this equation is filled in. What do Amish and manganese miners with PD have in common? The first reacts to hay dust with the inflammatory response. The second reacts to manganese exposure with it. As does the American exposed to aluminum in the air. Mercury leeching out of his dental work. The dust bunnies in the corners of his home. And so on.

But, one asks, so what? Is the body so sensitive to LPS that it will respond with collapse to the neuroinflammation? DSoes that not mark a species for extinction? I mean, we are saying that one is reacting to one of the most common substances in our environment by committing suicide, aren't we? And why would it take so darned long?

Those are sensible questions, I grant. But they are distractions because they fail to take into account the "rest of the story" - the power of the immune sysyem's messenger cells called cytokines. There are about 24 of these. Half of them cause an increase in the neuroinflammation and half a decrease. These are not ordinary cells with news from Upper Big Toe, Nebraska. These are the magic potions that allow the immune system to completely take over not only our bodies but our minds as well. The most common example and one with which we are all familiar is what is known as "sickness" behavior. You know, that urge to crawl away under a bush and just die? Or to whine for chicken soup? We don't usually think about it, but there you have one part of your brain taking the keys away from another.

So, we have the jihadist immune cells (microglia) gearing up to whip some invader butt; while the neuro system wanders around with open mouth and without a clue; while the endocrine system splashes its secretions around and like Sister Mary Oliphant keeps trying to get the classroom under control: while down at the GI Ranch the bunkhouse has been flooded with those darned cytokines that seem to be everywhere and which encourage a steady constipation as well as inflammation of the bowel and all the Nasties that it holds; while this gastroinflammation leads to a leaky gut poisoning the blood which then finds Ron's BBB and invades the CNS!

All this excess is normally balanced by the endocrine system and its magic glands through the use of an amazing device called the "feedback loop". Things start moving too fast? A moment with the Loop puts it to rights. Critical thresholds approaching? No problem. Just a tweak!

But somethings wrong. The saloon is in an uproar and someone shot the piano player. And Timmy is having little luck getting the attention of a grown up to tell him that the barn is on fire.

Now, THAT is Parkinson's Disease! :D

If you go back and brush away the fluff, you will find at least five systems taking part. Not simply being influenced or being buffeted about, but actually running up and down the hall with a hockey mask and a chainsaw!

I speak of "balance" quite a bit because that is what PD is all about. And I just don't mean the face-plant kind. I mean the type that has a highly adatable yet finely tuned creature ignoring the fact that he evolved in a womb of 24 hour periods endlessly repated. With half of it bathed in light. And not ordinary light, mind you, but light with the numbers precisely defined. So much so that you could design a miracle around it. Or at least you could until the early 1800s when artificial lighting came along with shift work in tow.

So Balance took a blow as people walked the smoggy streets in the dark going to thier dusty hell hole jobs. With no one to catch them if they fall through the safety net because they left the family structure (once again refecting 100,000s of years of teting to find what worked) back in the fields where their species was born. And where you began in the morning with the sun and went to bed with the moon and the time between was peaceful because your stresses were shortlived acute ones and not the soul-eating pressures of the chronic ones that never leave. And keep balance at bay all your life.

So much change and coming so fast tears at the soul. And like the canary in the coal mine, some of us get to warn the rest.

As to that book? I still intend to write it again. The first version was lost in a server crash some time back. The gist of it can be read at my blog at A Matter of Balance. Unexpected offers of cash are accepted and may be left in the cigar box at the right....:D

Can't get the site up through Wordpress. keeps closing down

Hmmm.. Seems alright from here.
 

Thelma-
Try it again and let us know. Anyone else had a problem?
-Rick

Wow what a reply.

There has been much debate on the impact of the Industrial Revolution on the standard of living. [1]

I think we can agree that the quality of life of the working class in England deteriorated in the early part of the Industrial Revolution. For instance [2]:
But, to link this to Parkinson's would require an association between poverty and the disease. In a naive sense the opposite is probably true: PD is associated with age; life expectancy is associated with wealth. However, if we take this confounding effect into account, we are left with the interesting question:

Is age adjusted PD incidence associated with wealth or poverty?

References

[1] "The Standard ofLiving Debate and the Industrial Revolution"
Kirby P.
Refresh 1997
http://www.ehs.org.uk/ehs/refresh/assets/Kirby25a.pdf

[2] "The Condition of the Working Class in England"
Engels F., 1845, reported in Wikipedia:
http://en.wikipedia.org/wiki/The_Con...***_in_England

John

I don't think we can ignore the records in ancient India given they have proven Ayurvedic treatment going back thousands of years. If you think of it (sobering as it is) we really are no further ahead given that we all are diagnosed on presenting symptoms, clinical observation, and response to treatment, so we cannot dismiss any account of PD on this basis.

There is a compelling logic to associating PD with the rise of industrial pollution, but Parkinson gives us only 6 case studies. We would need to know if these people lived or worked in and near factories. Charcot really is the one who put PD on the map with extensive studies beginning in 1861 that spanned 20 years. He and his students defined the cardinal signs; it would be fantastic if they collected patient data. The Industrial Revolution coincides with the birth of neurology and PD was just being defined as a bona fide disorder, so we cannot tell if there was an increase in incidence based on pollution or just that it was now being recognized more by doctors as a disease?

If we acknowledge Ayuraveda, there is some merit that PD was around in ancient times. This actually lends support to Rick's theory. It is easy to name a neurotoxin that bridges ancient to modern PD and likely connects much (if not all) neurodegenerative disease: that is chronic exposure to airborne metals. Early metallurgy (PD 2500 BC) evolves to pollution from smelting (19th c.) to addition of lead followed by Manganese to automobile fuel (20th century). Someone just needs to connect the dots... (not forgetting pesticides, but Round Up was a mere gleam in the early Industrialist's eye.)

I am thinking similar stats pop up across the world.

Fine-Particulate Air Pollution and Life Expectancy in the United States. NEJM 2009

didn't rome fall partially due to lead poisoning? people likely breathed in more particulate matter from living in huts, caves, buildings using wood to cook and heat than they did in industrial england, even if they lived in rural areas, especially in the winter.

smelting metals, especially tin, copper, lead ,silver and gold and all the accompanying metals including manganese must have created enough air pollution to cause some pd in miners at least a 1000 years ago? the ancient europeans, asians, africans and south americans did a lot of mining, ate a lot of rotten food, etc. i imagine many of the pigments used by the great masters weren't all that safe. what about all those fireplaces in english castles?

what was the avg lifespan in europe prior to the development of water sanitation and antibiotics?

just playing devil's advocate.

You are saying that if Parkinsonism can be correlated to inhaled toxins, then more PD would have been more prevalent throughout history? I am not sure what you mean. I do not think this is the only path to PD but just the only one, other than viral infection, that could connect us over a big span of time , but still within the context of Rick's thoughts on fallout of the Industrial Revolution.

The toxic soup we now breath is far different in content (pre automobile) and is far more pervasive. Plus, it is grossly unregulated. I think there is a huge difference between what was inhaled by cave dwellers using fire to what is inhaled when a Teflon pan overheats. Dupont had lots of explaining to do when people started losing their pet birds. They are still allowed to sell the crap but have added a disclaimer for the family parakeet.

As for life expectancy rates comparison, yes more people were lost to unsanitary living conditions and or no antibiotics, but I don't think we can make a direct comparison. It is common knowledge that life span has increased with vaccination and use of antiobiotics, but in this regard from an evolutionary perspective we all equally benefit from those things. We negate this gain by embracing "progress". We are exposing the human body to things it is not designed to handle, and we are the sorry outcome. We have a message no one wants to hear. I could cite numerous resources linking air pollution and disease, but I cannot be more clear than this doctor with the Physicians for Socially Responsible Medicine


The systemic inflammation caused by particulate pollution also affects the brain. Air pollution components reach the brain not only through the vascular system, but translocate via the nasal mucosa, along axons of the olfactory and trigeminal nerves into the central nervous system (CNS), allowing deep penetration into the parenchyma and brain stem (35, 36). Furthermore, many of the compounds adsorbed to particulate matter, like heavy metals, are neurotoxic. Through this mechanism, particulate pollution causes CNS oxidative stress, neuroinflammation, neuronal damage, cortical stress measured by EEG, enhancement of Alzheimer type-abnormal filamentous proteins, BBB changes, and cerebrovascular damage. Many of these changes can be found in children and young adults. Greater air pollution exposure is associated with lower intelligence, poorer motor function, attention deficits and behavioral problems in children, decreased cognition in adults, higher rates of strokes, multiple sclerosis, autism, Parkinson's and other neurodegenerative diseases (37, 38, 39, 40, 41, 42, 43, 44).


I hope this addresses what you mean?

your're preaching to the chorus laura, there's ample evidence that man made chemicals cause all sorts of diseases in humans and animals. kind of why we have the FDA, EPA.
almost impossible to get highly profitable chemicals banned without tremendously strong evidence. noone wants to put DOW, MONSANTO, BAYER, CHEVRON, DUPONT, etc. out of business.

my point was i didn't think the pre-industrial revolution environment was all that pristine 24hrs/day, 12months/year and pd likely existed.

I agree that it existed, but think it reasonable to assume that it became markedly worse and continues to "evolve" even now. The ultra-fine particulates are obvious suspects and are a little bit frightening once one takes a close look. They are "nanoparticles" and we are just now beginning to appreciate what a threat they may pose. For one thing they are so small that traditional barriers such as the BBB and the similar one lining the gut are pretty much ineffective. These guys are so small that a neuron looks like a super highway to them and they move along in both directions. They also are able to latch onto larger molecules and transport them across those barriers as well. As an irritant alone they are a constant source of inflammation plus they go deep into our lungs. They are, indeed, produced by burning wood but the smallest come from coal and diesel smoke. And they travel far with the wind. One area is called the "Alaskan Rectangle of Death" because global wind conentrates them north of Fairbanks. And remember that if the hypothyses (sp?) that I push is correct and it is about an inflammatory response to a number of possible triggers, that they would interact with most others to multiply their effects.
Rick

One way to mine data is to analyse past values to see if there are trends or cycles in the data or whether there are temporal correlations with other variables. I've made a start by looking at 12 years, 1999 to 2010, of monthly US mortality data.

The data comes from the multiple causes of deaths, Wonder database at the CDC.

The graph below shows the raw PD data (blue, lefthand scale) and raw all cause data (red righthand scale). The most noticeable features are:
- the variability from month to month;
- the values go through an annual cycle: high in winter, low in summer;
- the PD and all cause numbers follow similar patterns.

Attachment 7403

In the results shown below, the following terms are used:
PD: number of deaths with Parkinson's Disease as one of the multiple causes.
ALL: number of deaths from any cause.
DELTA: PD - ALL
RAW: unprocessed data from the query shown in the Data section.

1. Basic monthly statistics.
RAW PD: mean=2822, min=2156, max=3673
RAW ALL: mean=202611, min=180153, max=247828

2. Seasonality, distribution of deaths by month.
INDEX: processed data taking into account the number of days in each month, shown as an index centred on 100. For instance, if you had just January and February data from two years, the raw data could be Jan=310, Feb=280, whereas the index for both is 100.
SEQ: 12 values, one for each month, in order from January to December.
INDEX PD: mean = SEQ(115.6, 112.9, 108.9, 99.1, 93.1, 88.6, 88.2, 88.0, 92.6, 99.0, 103.4, 111.2)
INDEX ALL: mean= SEQ(110.2, 109.3, 106.3,100.4, 96.4, 94.2, 93.2, 92.5, 93.9, 97.4, 99.9, 106.6)
INDEX DELTA: mean = SEQ(5.4, 3.6, 2.6, -1.4, -3.3, -5.6, -5.0, -4.5, -1.2, 1.6, 3.5, 4.6)
Both the all cause and the PD mortality rates are higher in the winter than in the summer. (It would be interesting to know whether this is true in the southern states.) PD shows more seasonality than the all cause data.

3. Trend.
RAW PD: trend = +0.74%/year
RAW ALL: trend = +0.12%/year
Needs analysis, but I think this is most likely due to the ageing population, linked to the increasing prevalence with age of PD.

Statistical software
The calculations were done using a programming language called r (a free version of the long standing statistical programming language s). Its advantage is that it has an enormous library of statistical functions.

Data
The data comes from the Wonder database at the CDC. The database queries are shown in the Appendix.

Wonder does not require any programming skill to use. It is an excellent system, which I recommend to anyone with an interest in epidemiology. Although on this occasion I used a different approach, you can export the results in a file which can be imported into Excel.

"Dataset: Multiple Cause of Death, 1999-2010"
"Query Parameters:"
"Title:"
"Autopsy: All"
"Gender: All"
"Hispanic Origin: All"
"MCD - ICD-10 Codes: G20 (Parkinson's disease)"
"Place of Death: All"
"Race: All"
"States: All"
"Ten-Year Age Groups: All"
"UCD - ICD-10 Codes: All"
"Urbanization: All"
"Weekday: All"
"Year/Month: All"
"Group By: Month"
"Show Totals: True"
"Show Zero Values: False"
"Show Suppressed: False"
"Calculate Rates Per: 100,000"
"Rate Options: Default intercensal populations for years 2001-2009 (except Infant Age Groups)"
"---"
"Help: See http://wonder.cdc.gov/wonder/help/mcd.html for more information."
"---"
"Query Date: Mar 25, 2013 11:45:47 PM"
"---"
"Suggested Citation: Centers for Disease Control and Prevention , National Center for Health Statistics. Multiple Cause of Death"
"1999-2010 on CDC WONDER Online Database, released 2012. Data are from the Multiple Cause of Death Files, 1999-2010, as compiled"
"from data provided by the 57 vital statistics jurisdictions through the Vital Statistics Cooperative Program. Accessed at"
"http://wonder.cdc.gov/mcd-icd10.html on Mar 25, 2013 11:45:47 PM"
"---"

John

Is there a connection between the time of the year and Parkinson's?

This can be broken down to:

Do PwP perform better relative to controls at some times of the year than others?

Is there a correlation between the date of birth and PD?

Knowing the answer to these questions would give a good clue as to the aetiology of PD. It would also have implications for dosing and for clinical trials.

Using imaging technology, a team based in Finland report a seasonal variation in PD.

People tested fall and winter compared to those tested in the spring and summer have "15% higher tracer uptake". Those born during winter and spring cf summer and fall have from 8% to 16% higher uptake capacity depending on site [1].

They conclude:

"The results suggest that there are seasonal oscillations also in the hypoactive dopaminergic system of Parkinson's disease patients. Findings concerning season of birth further suggest that there may be gestational or perinatal seasonal factors, which influence dopaminergic function in adulthood".

But, Canadian researchers using epidemiological data find [2]:
"no evidence of systematic seasonal variation in PD incidence by birth date, or of clustering of birth dates during influenza pandemic years in PD patients".

References:

[1] "Seasonality of striatal dopamine synthesis capacity in Parkinson's disease"
Valtteri Kaasinena, Pekka Jokinenb, Juho Joutsaa, Olli Eskolab, Juha O. Rinneb
Neuroscience Letters, Nov 2012
http://www.sciencedirect.com/science...04394012012931

[2] "Is there seasonal variation in risk of Parkinson's disease?"
Postuma R. et al.
MovementDisorders, May 2007
http://onlinelibrary.wiley.com/doi/1...21272/abstract

John

Explain!

Since this thread started we have more data. The data below comes from the CDC Wonder database, which continues to live up to its name. The data shows the number of deaths in white males where PD was present for each year between 1999 and 2013.

"Year" Deaths Population Crude Rate
"1999" 7829 112695874 6.9
"2000" 8315 113445038 7.3
"2001" 8943 114582599 7.8
"2002" 9074 115381931 7.9
"2003" 9574 116075451 8.2
"2004" 9777 116912350 8.4
"2005" 10576 117707377 9.0
"2006" 10627 118555067 9.0
"2007" 10818 119363736 9.1
"2008" 11238 120168475 9.4
"2009" 11324 120882836 9.4
"2010" 12067 121403489 9.9
"2011" 12665 122321135 10.4
"2012" 13200 122937079 10.7
"2013" 14028 123559280 11.4
"Total" 160055 1775991717 9.0
"---"
"Dataset: Multiple Cause of Death, 1999-2013"
"Query Parameters:"
"Title:"
"2013 Urbanization: All"
"Autopsy: All"
"Gender: Male"
"Hispanic Origin: All"
"MCD - ICD-10 Codes: G20 (Parkinson's disease)"
"Place of Death: All"
"Race: White"
"Single-Year Ages: All"
"States: All"
"UCD - ICD-10 Codes: G20 (Parkinson's disease)"
"Weekday: All"
"Year/Month: All"
"Group By: Year"
"Show Totals: True"
"Show Zero Values: False"
"Show Suppressed: False"
"Calculate Rates Per: 100,000"
"Rate Options: Default intercensal populations for years 2001-2009 (except Infant Age Groups)"
"---"
"Help: See http://wonder.cdc.gov/wonder/help/mcd.html for more information."
"---"
"Query Date: Jul 29, 2015 11:19:07 AM"
"---"
"Suggested Citation: Centers for Disease Control and Prevention, National Center for Health Statistics. Multiple Cause of Death"
"1999-2013 on CDC WONDER Online Database, released 2015. Data are from the Multiple Cause of Death Files, 1999-2013, as compiled"
"from data provided by the 57 vital statistics jurisdictions through the Vital Statistics Cooperative Program. Accessed at"
"http://wonder.cdc.gov/mcd-icd10.html on Jul 29, 2015 11:19:07 AM"
"---"

John

Research [1, behind a paywall], based on data from Olmsted County, Minnesota, shows:

"the incidence of parkinsonism and PD may have increased between 1976 and 2005, particularly in men 70 years and older. These trends may be associated with the dramatic changes in smoking behavior that took place in the second half of the 20th century or with other lifestyle or environmental changes. However, the trends could be spurious and need to be confirmed in other populations."

Reference

[1] "Time Trends in the Incidence of Parkinson Disease"
Rodolfo Savica et al.
JAMA Neurology, June 2016
JAMA Network | JAMA Neurology | Time Trends in the Incidence of Parkinson Disease

John