As we approach the biggest feast of the year –THANKSGIVING meal-where we all sometimes tend to overindulge only to feel guilty afterwards – this year I want all of us to take advantage of the beautiful intrinsic system in place to boost our serotonin levels to help improve our sleep, bowel motility and our overall well-being.
We all know that those of us who battle Parkinson’s disease tend to suffer from low serotonin as seen in our poor sleep, constipation and frequent bouts of depression. This is because serotonin also known as 5 hydroxytryptamine (5-HTP) is in charge of regulating the mood, sleep, and in charge of many of our body’s vital functions.
We use to think that serotonin was primarily a brain neurochemical located primarily in the brainstem center (raphe nucleus) of vital organ control such as thermoregulation, sleep, pain response, and breathing. However, it turns out that 95% of the serotonin (50% of dopamine) in our bodies is made and located in our guts!
So that idea of having a “gut instinct” is more accurate than we thought. We are what we eat after all. There is a greater connection between the brain and the gut than we ever imagined. Does any one else get extremely irritable or migranous if they don’t eat on time? Usually starts about 15-30 minutes before feeding time. the only way to ward off this ugly monster from rearing its head is to feed it and feed it FAST! this is because our serotonin levels have hit rock bottom. It has been studied that low levels of serotonin sets off feelings of anger ( in the amygdala) and decreases the calming effect usually given by the pre-frontal lobe. So it turns out that those individuals who experienced fast /rapid depletion of serotonin can lead to people being more prone to aggression- maybe a reason why PD patients get more aggressive with intake of dopamine agonists. as we increase dopamine – invariably serotonin levels go down.
WHY is this?
Back at the beginning in our embryological development, the initial cells divided into the central nervous system and the enteric (gut) nervous system. Outside of the brain, the gut has the most neuron connections having an estimated 600 million neurons. Furthermore, the gut sends four times as many signals to the brain than vice versa. It is no wonder why many scientists and people believe not only the gut to be “the second brain,” but also as Japanese believe the midsection to be the ‘center of all wisdom,‘(physical and spiritual) also known as the HARA. So, when they say I know– they often point to their stomach just below the navel rather than their head as we would. Thus giving us a whole new insight into ‘gut feelings.’
The brain apparently is extremely active and is telling us more than we are discerning. The gut has its own set of intelligence which warns us in subtle ways like having butterflies, being nauseated, or even having knots in our stomach. Since so much serotonin and dopamine lie in our gut, we really must pay attention as to what we feed it to make it happy and in turn make us happy. More than ever it seems that the saying you are what you eat has greater significance and even more so for those of us who have Parkinson’s and chronic constipation and a whole host of other gi problems – it’s no wonder we feel sad, depressed, in pain and unable to sleep. The gut is also in sync with the brain during sleep as the brain cycles through 90 minutes of slow waves frequencies followed by rapid eye movements (REM) of dream state, the gut flows a similar pattern of 90 minute cycle of slow – wave contractions of the gut followed by brief rapid muscular movements strengthening the idea of a brain -gut connection.
WHAT can we do to keep our serotonin levels up for feeling of well- being?
Remember what we feed our stomachs also feeds our mind/brain.
Thus, this Thanksgiving and every meal we must make conscious effort to feed our guts the right nutrients that will help stimulate the release of serotonin for a happier you. Yes, it is true that Turkey has some quantities of tryptophan the precursor of serotonin but you would have to consume excessive amounts of this wonderfully delicious favorite national dish on an empty stomach to get some of its serotonin effects. Rather than trying to get all of your serotonin needs through a huge serving of Turkey this Thanksgiving ( and everyday of the year), I recommend a well-balanced meal. Turkey is not the only product rich in tryptophan. Other products which contain this chemical are :
- salmon (fatty fishes-i.e. sardines), eggs;
- fruits like bananas, tomatoes, plums, cherries, pineapple, and kiwi;
- according to the “journal of molecular medicine,” foods rich in B vitamins especially B6- cereals, rice and breads would be an excellent source.
- nuts- almonds, walnuts, even peanut butter, etc.
- CHOCOLATE- dark
Great serotonin enriched meal after Thanksgiving would be a turkey sandwich on enriched bread with tomatoes perhaps some fruit and or a piece of dark chocolate for dessert! (you know I will be doing my part this week of helping my brain by having a piece of chocolate pie after my turkey!)
A well -balanced diet full of carbs and proteins is your ticket to a happy new you – but first learn listen to your belly- it ALWAYS knows what it needs -feed it the right things and you too will be a much happier person despite Parkinson’s disease.
Have a Happy Thanksgiving Everyone & Many Blessings to All!
About a year before my dad passed away, he and I were at the store about to enter the store to do some grocery shopping when comes along a lady stooped at 90 degree angle pushing a buggy full of groceries. My heart immediately sank at this site. This lady apparently had been shopping all alone. I wonder how it was possible to live like this (bringing back memories of some of my dystonic patients further gripping my heart). Sensing my anguish, before I could say or do anything being completely paralyzed at the site of this phenomenal woman who ventured all alone despite the pain she must be have likely been enduring, my father quietly stated- “I so hate that you are sick.”
I turned and looked at him with intrigue in my eyes. “But dad that poor woman…” as I trailed off he said: “I know you are a great doctor and if you were working I bet you could help her get better.”
A lump formed in my throat thinking about this person and so many more that could use my skills as a doctor, after all I was nowhere near as disabled as this person in front of us.
Before I could get to her someone came and help her load her truck and I had to watch and see how she was going to drive. Sure enough as I though, when she climbed unto the vehicle and set down she was able to straighten up.
My dad was amazed at this. I explained to him this was a form of dystonia (abnormal sustained involuntary contraction of the muscles) called Camptocormia (a.k.a bent spine). This is a dystonic posturing linked to atrophy of the paraspinal muscles. This is posturing is known as one of the extreme postures impairments linked or associated with Parkinson’s disease (PD). Camptocormia in Parkinson’s is defined as extreme anteroflexion of the trunk which abates with recumbent position or standing up against a wall or hard surface. Thus this lady possibly had PD –dystonia at the very least. PD patients who have this tend to have early involvement of axial muscles and long duration of illness as well as tend be older of male gender with history of spondyloarthric spine increasing risk of developing camptocormia. This particular dystonia does not respond to levodopa or have very minimal response. Interestingly, the Pet scans looking at dopamine transporters of PD patients with and without Camptocormia are identical.
Although dad knew little of neurology or dystonia he had a good 6th sense and was correct in assuming this woman’s condition was in my area of expertise. I frequently think of both that lady who I have not seen again and my dad who is now gone to be with the Lord. Yet, the resolve to understand the connection between the two movement disorders in an attempt to find relief to so many people in need has only strengthen with time.
There are two other dystonic syndromes involving the AXIAL muscles commonly seen by MDS that are frequently related to parkinsonian patients:
- Head drop (anterocollis- cervical dystonia)
- Pisa Syndrome- a condition in which there is sustained involuntary flexion of the body and head to one side and slight rotation of the trunk when sitting and standing. This gives the appearance of leaning tower of Pisa – hence the name! This condition also commonly seen in schizophrenia.
These two are typically related to Multisystem atrophy (MSA)! However, Pisa syndrome can be seen infrequently in PD as well. Those that have this syndrome tend to have lower body mass index; higher disability due to longer duration of disease and more advanced disease. Subsequently, PD patients with Pisa syndrome had poorer quality of life partly due to increased falling. Severe osteoporosis and arthrosis were significantly part of the life of these patients as well. Although, anterocollis is a sin-qua- non of MSA in its early presentation but when it occurs in the late stages of PD it is invariably due to medication effect (wearing off).
Despite the fact that dystonia is the third most common movement disorder after essential tremors (ET) and PD is still not well recognized or understood; even though there have been many advances in the last several decades identifying specific genes causing dystonic syndromes.
One of the main problems in dealing with dystonia from a medical point of view is that it is both a symptom as well as a diagnosis of primary neurological disease. This notion has always intrigued me particularly after I developed YOPD and my initial symptoms as it is common in the majority of YOPD to commence with some sort of focal dystonia. Despite the fact that I have been trying for a number of years to get the Parkinson’s foundations to work side by side the dystonia foundation to focus on the common path ways. After a decade, I am happy to report progress by a final acknowledgement of dystonia as a presenting symptoms of PD by the MJfox foundation. Further, they are beginning to recognize a pattern of presentation which is essential in the diagnostic armamentarium of every physician (who depend on pattern recognition) but also for the PD community to be aware of the possible initial symptoms.
Keeping above in mind we also have to remember that dystonia itself is not a common /classic presenting symptom of PD. However, when it is the presenting symptoms it’s in YOPD. In YOPD, dystonia is more commonly isolated in the lower limb as it was my presenting symptom. As a symptom in general isolated lower limb dystonia is very rare in adults. This dystonia is also referred as kinesigenic foot dystonia this is because this type of dystonia is brought on by exercise and/ or movement of the foot- typically causing toes to curl involuntarily and sometimes exaggerated hyperflexion of foot causing much pain and discomfort.
Common trigger is putting on shoes for women particularly if attempting to put on high heels as they cause us to arch our foot even further.
Treatments: Vary depending on cause
As with any illness – the key to successful treatment is first deciding its cause- whether the dystonia in any individual is a symptom of an underlying neurological disease or a disease itself such as primary dystonia or Dopa- responsive -dystonia (DRD)?
Once you have ascertained that these syndromes are part of Parkinson’s or Parkinson’s plus disorders then we must consider their treatment.
- Anterocollis– Commonly causes neck pain and cervical radiculopathy. Botox works wonders; adjusting PD meds; therapy, cervical collar & DBS. Must recognize and treat early before cervical damage can occur and or cause fracture of c-spine!
- Pisa syndrome– Commonly causes back pain. Discontinue using antipsychotic drugs and usage of amantadine and other anti-cholinergics; no good treatment for those caused by neuroleptics.
- Camptocormia- Commonly causes back pain and lumbar/thoracic radiculopathy. Since levodopa has little or no effect we must consider alternative treatments. These include: withdrawal of causative drugs like antipsychotics or neuroleptic drugs such as Haldol; orthotic aids; Physical therapy; steroid injections; Botox injections which have proven of great value in many patients with this type of dystonia- would be my first choice after excluding triggering causes/medical causes; muscle relaxants – baclofen, dantrolene, etc.; tetrabenazine; amantadine; and surgical intervention -such as DBS- deep brain stimulation- subthalamic
- Lower limb dystonia– start dopamine agonists; levodopa; physical therapy; foot orthotics; Botox; muscle relaxants; DBS when necessary.
In summary having one of the first 3 syndromes in the presence of PD is a sign of disabling advanced disease leading to higher comorbidities which in turn can lead to spine fractures of neck and back requiring surgery if not properly treated and managed early in its presentation. The latter two frequently result in severe falls due to loss of balance and “veering” of gait. However, presence of lower limb dystonia in a young adult could signify the onset of Parkinson’s disease. Thus, need to follow up with a neurologist/ MDS for all these types of dystonia for a better prognosis and quality of life.
Dolhun, R. The Michael J. Fox foundation for Parkinson’s Research. (September 2015) :”Dystonia and Parkinson’s Disease.” Practical Neurology. 14(7):43-46.
Source: Seasons of Support! By Maria De Leon
Source: Feeling Distressed Today? by Maria De Leon