Parkinson’s disease has always been primarily seen as a movement disorder resulting in symptoms of shaking, tremors, rigidity, and trouble walking. Interestingly, however, at least 90% of patients with Parkinson’s experience either loss or decreases in the sense of smell. Studies have shown that problems with olfaction actually generally precede the onset of other motor symptoms. Most people are not personally aware of changes in their olfactory acuity, but the increasing range and prevalence of smell tests offer a quick, easy, cheap, and non-invasive diagnostic test, as well as a measure of disease progression. In addition, the shift of focus for researchers from Parkinson’s as a motor disorder to a more global neurodegenerative disorder allows consideration of new paradigms about the causes and disease progression.
The cellular basis of olfactory dysfunction in Parkinson’s remains an enigma. Post-mortem studies have confirmed shrinkage of the olfactory bulb, but this fails to shed light onto the root causes as it only demonstrates the end effect. Experimental models of Parkinson’s have demonstrated various results such as protein aggregation in the olfactory bulb, changes in levels of neurotransmitters, microglial activation, and loss of cells in the olfactory bulb. However, as all of these effects are inter-related, none of these clarify the actual initial cause of damage.
Many of the hypotheses as to why olfactory dysfunction occurs and precedes other symptoms remain grounded in the long-held paradigm of Parkinson’s as a motor disease caused by the loss of dopaminergic neurons in the substantia nigra. For example, in some experimental models an increase in dopamine was found in the olfactory bulb. The researchers suggested this occurs as a compensatory mechanism in response to the loss of dopamine in the substantia nigra. As it has also been shown that sense of smell is particularly vulnerable to changes in dopamine, excess dopamine in the olfactory bulb would, thus, lead to olfactory dysfunction.
However, a number of other theories have been proposed suggesting that perhaps the olfactory bulb is the first brain structure to exhibit signs of damage because Parkinson’s could be caused by respiratory viruses or inhaled toxins that enter the brain through the nose. The cause of Parkinson’s has not been conclusively determined. And while a genetic component has been uncovered, the causes are clearly much more complex with various environmental factors involved. A number of studies have been performed demonstrating Parkinson’s-like symptoms following exposure to viruses, heavy metals, and pesticides in experimental models. Epidemiological studies have also linked pesticides exposure to an increased risk of Parkinson’s. It is certainly an interesting hypothesis that inhaled toxins could cross the blood brain barrier, and that the damage in Parkinson’s could begin first in the olfactory bulb and then spread from there to the substantia nigra. In addition, as the olfactory bulb is heavily involved in adult neurogenesis, any damage to this structure could severely limit the brain’s ability to repair itself by replenishing damaged neurons with new ones. Perhaps, then, Parkinson’s disease does not depend on a single source of damage, but rather multiple insults occurring. For example, genetically induced damage to the dopaminergic neurons in the substantia nigra combined with inhaled toxins damaging the olfactory bulb could, together, cause Parkinson’s, while one or the other would be insufficient.

Judging from those hoaky commercials, some products will transform you from a jellyfish into a superhero in a jiffy. But what about the mantra we’re hearing that aggressive weight loss is hopeless, because it results in rebound weight gain? Our brain’s reward centers, our hormones, and our psyches simply can’t resist the evolutionary forces unleashed by artificial famine conditions, they say.
Some research is telling us that people can lose weight fast and that this speedy start bodes well for sustained improvement: More weight loss, and no more rebound than slower dieters that lose less weight. This has been a recurring outcome, even recently. Posts online make the claim more boldly than the researchers. A look past the headlines tells us a more nuanced story.
In a study by Nackers and colleagues, three groups were identified: fast, medium, and slow. The fast group lost more weigh up front, and kept it off just as successfully as the other groups. But this does not mean that an aggressive calory restriction diet is the answer. Here are some points to consider.
The fast group did not consume a drastically lower number of calories than the slow one (1,366.4 vs 1,486.8).
The fast group did not lose a drastic amount of weight, compared to the slow group (13.5 vs. 5.1 kg). Yes, it’s more than double, but it’s over six months.
We should ask what distinguished the slow group from the rest. The slow group attended less meetings, exercised less, and ate more calories. Were they more stressed? Was there a higher rate of depression? Where there other conditions that made them less active? Something was going on. Since the slow group was not as successful at maintaining weight loss, it’s a good guess that the conditions continued throughout the study period. The fast group was 5.1 times more likely to have maintained at least a 10% weight loss at 18 months than the slow group.
There are countless factors that might interfere. One is ADD. There is speculation that people with ADD have higher rates of obesity because their reward system is especially in need of a dopamine fix, and because of less consistent self-discipline. Medication appears to remedy this for many folks.
If there’s a take away, it seems that it would be for us to ask ourselves what might keep us from fully participating in a weight loss program. Those factors are probably the gateway to significant, sustained weight loss.